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        <title>Innate Immunity via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Innate Immunity' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Innate+Immunity&t=Innate+Immunity&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 06:42:53 +0100</lastBuildDate>
        <item>
            <title>Lyn kinase controls TLR4-dependent IKK and MAPK activation modulating the activity of TRAF-6/TAK-1 protein complex in mast cells.</title>
            <link>http://www.medworm.com/index.php?rid=5659828&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22302035%26dopt%3DAbstract</link>
            <description>Authors: Avila M, Martinez-Juarez A, Ibarra-Sanchez A, Gonzalez-Espinosa C
    Abstract
    Mast cells (MCs) control allergic reactions and contribute to protective innate immune responses through TLR4 activation. The tyrosine kinase Lyn is important to the high affinity IgE receptor (FcÎµRI) signal transduction system in MCs, but its role on the TLR4 signalling cascade is still elusive. Here, we characterized several TLR4-triggered responses in bone marrow-derived mast cells (BMMCs) from wild-type (WT) and Lyn(-/-) mice. We found that Lyn(-/-) MCs secreted lower amounts of TNF-Î± after LPS challenge when compared with WT cells. Lyn(-/-) BMMCs showed less MAPK, IÎºB phosphorylation and NF-ÎºB nuclear translocation after TLR-4 triggering than WT cells. LPS-induced MAPK and inhibitor of IÎºB...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5659828</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5659828</guid>        </item>
        <item>
            <title>Investigation of bacterial resistance to the immune system response: Cepacian depolymerisation by reactive oxygen species.</title>
            <link>http://www.medworm.com/index.php?rid=5642531&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22278934%26dopt%3DAbstract</link>
            <description>Authors: Cuzzi B, Cescutti P, Furlanis L, Lagatolla C, Sturiale L, Garozzo D, Rizzo R
    Abstract
    Reactive oxygen species (ROS) are part of the weapons used by the immune system to kill and degrade infecting microorganisms. Bacteria can produce macromolecules, such as polysaccharides, that are able to scavenge ROS. Species belonging to the Burkholderia cepacia complex are involved in serious lung infection in cystic fibrosis patients and produce a characteristic polysaccharide, cepacian. The interaction between ROS and bacterial polysaccharides was first investigated by killing experiments, where bacteria cells were incubated with sodium hypochlorite (NaClO) with and without prior incubation with cepacian. The results showed that the polysaccharide had a protective effect towards bact...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642531</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5642531</guid>        </item>
        <item>
            <title>6-Mer hyaluronan oligosaccharides increase IL-18 and IL-33 production in mouse synovial fibroblasts subjected to collagen-induced arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5642530&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22278935%26dopt%3DAbstract</link>
            <description>Authors: Campo GM, Avenoso A, D'Ascola A, Scuruchi M, Prestipino V, Calatroni A, Campo S
    Abstract
    Hyaluronan (HA) oligosaccharides stimulate pro-inflammatory responses in different cell types by modulating both cluster determinant 44 (CD44) and TLR4. The activation of these receptors is also mediated by collagen-induced arthritis (CIA) that, via two different pathways, culminates in the liberation of NF-ÎºB. This then stimulates the production of pro-inflammatory cytokines, including IL-18 and IL-33, that are greatly involved in rheumatoid arthritis. The aim of this study was to investigate the effects of 6-mer HA oligosaccharides on mouse synovial fibroblasts obtained from normal DBA/J1 mice or mice subjected to CIA. Compared with normal synovial fibroblasts (NSF), rheumatoid arth...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642530</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5642530</guid>        </item>
        <item>
            <title>Repeated oral administration of lipopolysaccharide from Escherichia coli 0111:B4 modulated humoral immune responses in periparturient dairy cows.</title>
            <link>http://www.medworm.com/index.php?rid=5624572&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266418%26dopt%3DAbstract</link>
            <description>The objective of this study was to evaluate the effects of repeated oral exposure to LPS on humoral immune responses of periparturient dairy cows. Sixteen Holstein cows were assigned to two treatment groups 2 wk before the expected day of parturition. Cows were administered orally, twice weekly at wk -2, -1 and +1 around parturition, with the following treatments: 3 ml saline; or 3 ml of saline containing LPS from Escherichia coli 0111:B4. The amount of LPS administered during wk -2, -1, and +1 was 0.01, 0.05, or 0.1 Âµg/kg body weight, respectively. Multiple blood samples were collected by jugular vein and various immune and clinical variables were measured. Results indicated that, on one hand, concentrations of plasma IgG anti-LPS Abs decreased (P &amp;lt; 0.01) and those of IgM anti-LPS Abs...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624572</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624572</guid>        </item>
        <item>
            <title>Diphenyl diselenide-modulation of macrophage activation: Down-regulation of classical and alternative activation markers.</title>
            <link>http://www.medworm.com/index.php?rid=5561822&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22215443%26dopt%3DAbstract</link>
            <description>Authors: Rupil LL, de Bem AF, Roth GA
    Abstract
    Diphenyl diselenide (PhSe)(2), a simple organoselenium compound, possesses interesting pharmacological properties that are under extensive research. As macrophages respond to microenvironmental stimuli and can display activities engaged in the initiation and the resolution of inflammation, in the present report we describe the ability of (PhSe)(2) to modulate the macrophage activation. Our data indicate that (PhSe)(2) could inhibit the NO production in a dose-dependent fashion in peritoneal macrophages activated by LPS or treated with vehicle alone. We could demonstrate that this effect correlated with a reduction in the expression of the inducible NO synthase in (PhSe)(2)-treated cells. Furthermore, (PhSe)(2) suppressed the production...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5561822</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5561822</guid>        </item>
        <item>
            <title>Letter to the Editor and response.</title>
            <link>http://www.medworm.com/index.php?rid=5536704&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22159048%26dopt%3DAbstract</link>
            <description>Authors: McPhee JB, Bliska JB
    PMID: 22159048 [PubMed - in process] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536704</comments>
            <pubDate>Sat, 24 Dec 2011 10:48:02 +0100</pubDate>
            <guid isPermaLink="false">5536704</guid>        </item>
        <item>
            <title>Activation of endothelial TLR2 by bacterial lipoprotein upregulates proteins specific for the neutrophil response.</title>
            <link>http://www.medworm.com/index.php?rid=5536700&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22186927%26dopt%3DAbstract</link>
            <description>This study suggests that endothelial TLR2 may be an important regulator of neutrophil trafficking to sites of infection in general, and that direct activation of lung endothelial TLR2 may contribute to acute lung injury during sepsis.
    PMID: 22186927 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536700</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536700</guid>        </item>
        <item>
            <title>LPS from Neisseria meningitidis is crucial for inducing monocyte- and microparticle-associated tissue factor activity but not for tissue factor expression.</title>
            <link>http://www.medworm.com/index.php?rid=5536703&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22180561%26dopt%3DAbstract</link>
            <description>Authors: OvstebÃ¸ R, Dalsbotten Aass HC, Haug KB, Siebke TrÃ¸seid AM, Gopinathan U, Kierulf P, Berg JP, Brandtzaeg P, Henriksson CE
    Abstract
    Neisseria meningitidis causes sepsis with coagulopathy. The present study evaluated the tissue factor (TF)-inducing capacity of bacterial LPS in different presentation forms, i.e. membrane-bound LPS versus purified LPS, and of non-LPS components of N. meningitidis. By using a wild-type N. meningitidis, a mutant N. meningitidis lacking LPS (LPS-deficient N. meningitidis), purified LPS from N. meningitidis and Escherichia coli, we measured TF-expression and TF-activity on human monocytes and microparticles (MPs). The effect of TF-modulators, such as phosphatidylserine (PS), tissue factor pathway inhibitor (TFPI) and recombinant IL-10 (rhIL-10) w...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536703</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536703</guid>        </item>
        <item>
            <title>Cigarette smoke induces growth differentiation factor 15 production in human lung epithelial cells: Implication in mucin over-expression.</title>
            <link>http://www.medworm.com/index.php?rid=5536702&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22180562%26dopt%3DAbstract</link>
            <description>Authors: Wu Q, Jiang D, Chu HW
    Abstract
    Excessive mucus is a hallmark of chronic obstructive pulmonary disease (COPD). There is an emerging interest in the role of TGF-Î² signaling in the initiation and progression of COPD. Growth differentiation factor 15 (GDF15) is a divergent member of TGF-Î² superfamily. However, whether cigarette smoke induces airway epithelial GDF15 production and its functions in the airways have not been revealed. Therefore, we first analyzed GDF15 protein expression in airway epithelium of human COPD smokers versus normal non-smokers. We then examined the regulation and function of GDF15 in human airway epithelial cells in response to cigarette smoke exposure. We found increased GDF15 protein expression in airway epithelium (mainly in ciliated cells) of hu...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536702</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536702</guid>        </item>
        <item>
            <title>Enhancement of the acute phase response to a lipopolysaccharide challenge in steers supplemented with chromium.</title>
            <link>http://www.medworm.com/index.php?rid=5536701&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22180563%26dopt%3DAbstract</link>
            <description>Authors: Burdick NC, Bernhard BC, Carroll JA, Rathmann RJ, Johnson BJ
    Abstract
    The study examined the effect of chromium supplementation on the response of steers to an LPS challenge. Steers received a premix that added 0 (control; n = 10) or 0.2 mg/kg of chromium (n = 10) to the total diet on a dry matter basis for 56 d. Steers were fitted with jugular catheters and rectal temperature (RT) recording devices on d 52. Blood samples were collected and sickness behavior scores assigned to each steer relative to an LPS challenge (0.5 Âµg/kg) on d 55. Pre-LPS RT were greater in chromium-supplemented than in control steers. Post-LPS RT increased in both treatments, with control steers producing a greater change in RT than chromium-supplemented steers. Sickness behavior scores were greate...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536701</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536701</guid>        </item>
        <item>
            <title>Mycobacterium bovis bacilli Calmette-Guerin regulates leukocyte recruitment by modulating alveolar inflammatory responses.</title>
            <link>http://www.medworm.com/index.php?rid=5423108&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22058091%26dopt%3DAbstract</link>
            <description>In this study, we used the Transwell model to investigate the mechanisms behind mycobacteria-induced leukocyte recruitment and investigated the role of TLR2 and TLR4 in this process. Infection of epithelial cells resulted in significantly increased secretion of the neutrophil chemotactic CXCL8 and IL-6, but no secretion of monocyte chemotactic CCL2 or TNF-Î± was observed. In contrast to epithelial response, mycobacteria-infected neutrophils and monocytes secreted all these cytokines. Corresponding with epithelial cytokine response, mycobacterial infection of the epithelial cells increased neutrophil diapedesis, but decreased monocyte recruitment. However, monocyte recruitment towards mycobacteria infected epithelial cells significantly increased following addition of neutrophil pre-conditi...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5423108</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5423108</guid>        </item>
        <item>
            <title>Cellular resistance to HIV-1 infection in target cells coincides with a rapid induction of X-DING-CD4 mRNA: Indication of the unique host innate response to virus regulated through function of the X-DING-CD4 gene.</title>
            <link>http://www.medworm.com/index.php?rid=5381835&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22042911%26dopt%3DAbstract</link>
            <description>Authors: Shilpi RY, Sachdeva R, Simm M
    Abstract
    Clinical reports indicate that some infected individuals control HIV-1 replication through undefined mechanisms. Our group reported that a human protein named X-DING-CD4 holds a potent antiviral activity, blocking transcription of HIV-1 LTR through the inhibition of NF-ÎºB/DNA binding. Based on observations that transformed HIV-1 resistant CD4(+) T cells produce higher levels of soluble X-DING-CD4 protein upon their exposure to virus, we hypothesized that resistance to HIV-1 in these cells may be regulated through function of the X-DING-CD4 gene. Real-time PCR evaluations of X-DING-CD4 mRNA expression confirmed our hypothesis; HIV-1 exposure caused rapid up-regulation of X-DING-CD4 mRNA in resistant, but not susceptible, cells; and th...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5381835</comments>
            <pubDate>Mon, 31 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5381835</guid>        </item>
        <item>
            <title>Fever induction by systemic stimulation with macrophage-activating lipopeptide-2 depends upon TLR2 but not CD36.</title>
            <link>http://www.medworm.com/index.php?rid=5381834&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22042912%26dopt%3DAbstract</link>
            <description>This study was designed to test the responses of TLR2-knockout mice (TLR2-KO) and wild- type mice (C57/BL-6), and of CD36 deficient spontaneously hypertensive rats (SHR) and their genetic controls [Wistar Kyoto (WKY) rats] to systemic stimulations with the TLR2/6 agonist MALP-2 and the TLR4 agonist LPS. Fever and formation of TNF-Î± and IL-6 induced by intraperitoneal injections of MALP-2 (1000 Âµg/kg) were completely blunted in TLR2-KO, while LPS (100 Âµg/kg)-induced responses were not abolished in these animals. In SHR lacking CD36, a reduction of fever was observed in response to MALP-2 (100 Âµg/kg), but LPS-fever was even more attenuated in SHR when compared with WKY controls. Concentrations of circulating IL-6 tended to be lower in SHR after stimulation with both pyrogens. However, th...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5381834</comments>
            <pubDate>Mon, 31 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5381834</guid>        </item>
        <item>
            <title>Native X-DING-CD4 protein secreted by HIV-1 resistant CD4+ T cells blocks activity of IL-8 promoter in human endothelial cells infected with enteric bacteria.</title>
            <link>http://www.medworm.com/index.php?rid=5381836&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22031506%26dopt%3DAbstract</link>
            <description>This study provides evidence that the X-DING-CD4 protein might be developed as a novel biotherapeutic to control LPS-mediated inflammation in advanced HIV disease.
    PMID: 22031506 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5381836</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5381836</guid>        </item>
        <item>
            <title>Single nucleotide polymorphism -799C/T in matrix metalloproteinase-8 promoter region in arterial disease.</title>
            <link>http://www.medworm.com/index.php?rid=5346118&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21994255%26dopt%3DAbstract</link>
            <description>Authors: Pradhan-Palikhe P, Pussinen PJ, Vikatmaa P, Palikhe A, KivimÃ¤ki AS, LepÃ¤ntalo M, Salo T, Sorsa T
    Abstract
    Arterial disease is associated with elevated serum matrix metalloproteinase (MMP)-8 concentration. We studied the role of two promoter region single nucleotide polymorphisms (SNPs) of MMP-8 gene in the arterial disease. The population comprised patients with arterial disease (n = 124) and healthy blood donors (n = 100) as a reference group for MMP-8 SNPs (-799C/T and -381A/G) genotypes and serum concentrations. Genotype frequencies for MMP-8 -799C/T SNP in arterial disease were C/C (43.5%), C/T (32.3%) and T/T (24.2%), and in the reference group they were C/C (50.0%), C/T (40.0%) and T/T (10.0%; P = 0.012). The -799C allele frequency was lower in the patients (59.7%)...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346118</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346118</guid>        </item>
        <item>
            <title>High variability of TLR4 gene in different ethnic groups in Iran.</title>
            <link>http://www.medworm.com/index.php?rid=5346117&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21994256%26dopt%3DAbstract</link>
            <description>Authors: Ioana M, Ferwerda B, Farjadian S, Ioana L, Ghaderi A, Oosting M, Joosten LA, van der Meer JW, Romeo G, Luiselli D, Dediu D, Netea MG
    Abstract
    Infectious diseases exert a constant evolutionary pressure on the innate immunity genes. TLR4, an important member of the TLR family, specifically recognizes conserved structures of various infectious pathogens. Two functional TLR4 polymorphisms, Asp299Gly and Thr399Ile, modulate innate host defense against infections, and their prevalence between various populations has been proposed to be influenced by local infectious pressures. If this assumption is true, strong local infectious pressures would lead to a homogeneous pattern of these ancient TLR4 polymorphisms in geographically-close populations, while a weak selection or genetic ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346117</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346117</guid>        </item>
        <item>
            <title>Chemokine release by neutrophils in chronic obstructive pulmonary disease.</title>
            <link>http://www.medworm.com/index.php?rid=5346116&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21997704%26dopt%3DAbstract</link>
            <description>Authors: Blidberg K, Palmberg L, DahlÃ©n B, Lantz AS, Larsson K
    Abstract
    Neutrophils are among the first cells to arrive at the site of injury. Chemokines secreted by neutrophils affect the migration of both neutrophils and other inflammatory cells, such as monocytes. It has been reported that LPS-induced release of IL-8 (CXCL-8) by neutrophils is amplified by neutrophil-derived TNF-Î±. We hypothesize that chemokine release by neutrophils is altered in chronic obstructive pulmonary disease (COPD) compared with healthy controls and that TNF-Î± may be involved in this alteration. Peripheral blood neutrophils isolated from smokers with COPD (n = 12), smokers without COPD (n = 12) and healthy, non-smokers (n = 12) were stimulated with LPS, TNF-Î± or organic dust. Anti-TNF-Î± Ab (inflix...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346116</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346116</guid>        </item>
        <item>
            <title>Endotoxin{middle dot}albumin complexes transfer endotoxin monomers to MD-2 resulting in activation of TLR4.</title>
            <link>http://www.medworm.com/index.php?rid=5346120&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21994253%26dopt%3DAbstract</link>
            <description>Authors: Esparza GA, Teghanemt A, Zhang D, Gioannini TL, Weiss JP
    Abstract
    Response to Gram-negative bacteria (GNB) is partially mediated by the recognition of GNB-derived endotoxin by host cells. Potent host response to endotoxin depends on the sequential interaction of endotoxin with lipopolysaccharide binding protein (LBP), CD14, MD-2 and TLR4. While CD14 facilitates the efficient transfer of endotoxin monomers to MD-2 and MD-2Â·TLR4, activation of MD-2Â·TLR4 can occur in the absence of CD14 through an unknown mechanism. Here, we show that incubation of purified endotoxin (E) aggregates (E(agg), M        (         r        ) â‰¥ 20 million) in PBS with â‰¥ 0.1% albumin in the absence of divalent cations Ca(2+) and Mg(2+), yields EÂ·albumin complexes (M        (         r        ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346120</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346120</guid>        </item>
        <item>
            <title>Effects of lithium on lipopolysaccharide-induced inflammation in rat primary glia cells.</title>
            <link>http://www.medworm.com/index.php?rid=5346119&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21994254%26dopt%3DAbstract</link>
            <description>In this study, we examined the effects of lithium on LPS-induced inflammation in rat primary glia cells. Cells were pre-treated with lithium (1 or 10 mM) for 6 or 24 h, after which, inflammation was induced by the addition of LPS (for another 18 h) to the culture medium. Thereafter, medium was collected and cells were harvested for further analyses. Levels of TNF-Î±, IL1-Î² and PGE(2) were determined by ELISA and NO levels by the Griess reaction assay. Expression levels of cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) were examined by Western blot analysis. We found that pre-treatment with lithium 10 mM (but not 1 mM) significantly reduced LPS-induced secretion of TNF-Î±, IL1-Î², PGE(2) and NO. In addition, lithium significantly reduced the expression of COX-2 and iNOS. These f...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346119</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346119</guid>        </item>
        <item>
            <title>Lipopolysaccharide pretreatment of the udder protects against experimental Escherichia coli mastitis.</title>
            <link>http://www.medworm.com/index.php?rid=5346121&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21990573%26dopt%3DAbstract</link>
            <description>Authors: Petzl W, GÃ¼nther J, Pfister T, Sauter-Louis C, Goetze L, von Aulock S, Hafner-Marx A, Schuberth HJ, Seyfert HM, Zerbe H
    Abstract
    Exposure to pathogen-associated molecular patterns such as LPS can cause an immune refractory state in mammals known as endotoxin tolerance (ET), resulting in a decreased inflammatory response after pathogen contact. This ET concept was used to reduce the severity of an experimentally-induced clinical mastitis. Cows were pretreated with 1 Âµg LPS per udder quarter and challenged 72 h (group L72EC) or 240 h (group L240EC) later with 500 CFU Escherichia coli. Pretreated animals showed no leukopenia after challenge, no (L72EC), or only slightly (L240EC), elevated body temperature and significantly reduced systemic and local clinical scores compared...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5346121</comments>
            <pubDate>Tue, 11 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5346121</guid>        </item>
        <item>
            <title>Indigenous New Zealand honeys exhibit multiple anti-inflammatory activities.</title>
            <link>http://www.medworm.com/index.php?rid=5298711&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21978989%26dopt%3DAbstract</link>
            <description>Authors: Leong AG, Herst PM, Harper JL
    Abstract
    Recent evidence suggests a potential role for honeys in mediating clinical inflammation and tissue damage. Here, we investigated the anti-inflammatory activity of a selection of previously untested indigenous New Zealand (NZ) honeys. We found that several, but not all, New Zealand rewarewa, manuka and kanuka honey samples exhibited potent, dose-dependent reduction of human neutrophil superoxide production in vitro. This inhibitory activity did not correlate with levels of known phenolic-based free radical scavengers. Furthermore, the active honeys did not scavenge superoxide generated in a cell-free xanthine/xanthine oxidase assay. In C57BL/6 J mice, topical application of manuka and rewarewa honey samples with the highest in vitro ac...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5298711</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5298711</guid>        </item>
        <item>
            <title>Inhibition of nicotinamide phosphoribosyltransferase modifies LPS-induced inflammatory responses of human monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5298712&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21975728%26dopt%3DAbstract</link>
            <description>Authors: Schilling E, Wehrhahn J, Klein C, Raulien N, Ceglarek U, Hauschildt S
    Abstract
    Recent studies have identified enzymes that use NAD as a substrate, thus contributing to its net consumption. To maintain the intracellular pool, NAD is re-synthesized by a salvage pathway using nicotinamide, the by-product generated by the enzymatic cleavage of NAD. Enzymes involved in NAD re-synthesis include nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase. Our studies show, that NAMPT was substantially up-regulated by LPS in primary human monocytes, suggesting that it may be especially required during the process of monocyte activation. To evaluate the contribution of the NAD rescue pathway to LPS-induced biological responses in human monocyt...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5298712</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5298712</guid>        </item>
        <item>
            <title>Mitogen-activated protein kinases p38 and ERK1/2 regulated control of Mycobacterium avium replication in primary murine macrophages is independent of tumor necrosis factor-{alpha} and interleukin-10.</title>
            <link>http://www.medworm.com/index.php?rid=5282210&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682586%26dopt%3DAbstract</link>
            <description>Authors: Klug K, Ehlers S, Uhlig S, Reiling N
    Abstract
    In macrophages, mitogen-activated protein kinases (MAPK) are critical regulators of both, mycobacterial replication and mycobacteria-induced cytokine formation. To segregate direct effects of MAPK function on mycobacterial replication from indirect, cytokine-mediated effects, we studied the growth of Mycobacterium avium strains in wild-type and tumor necrosis factor (TNF)-Î±- or interleukin (IL)-10-deficient bone marrow-derived murine macrophages. Using specific inhibitors of the p38- and the ERK1/2-MAPK pathways, we found that the use of SB203580 always reduced, whereas the presence of PD98059 always promoted, bacterial replication of highly virulent and intermediately virulent M. avium strains, independent of endogenous TNF-Î...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282210</comments>
            <pubDate>Tue, 04 Oct 2011 16:20:02 +0100</pubDate>
            <guid isPermaLink="false">5282210</guid>        </item>
        <item>
            <title>Downregulation of CXCL12 signaling and altered hematopoietic stem and progenitor cell trafficking in a murine model of acute Anaplasma phagocytophilum infection.</title>
            <link>http://www.medworm.com/index.php?rid=5282207&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21964802%26dopt%3DAbstract</link>
            <description>Authors: Johns JL, Borjesson DL
    Abstract
    Infection with a variety of bacterial pathogens results in hematopoietic stem and progenitor cell (HSPC) mobilization. The mechanism and kinetics of HSPC mobilization during infection are largely unknown. Previously, we found altered HSPC activity in bone marrow, spleen and blood during infection with Anaplasma phagocytophilum, the agent of granulocytic anaplasmosis. We hypothesized that altered CXCL12/CXCR4 signaling, a central pathway for HSPC homing to, and retention within, the bone marrow, plays a role in infection-induced alterations in HSPC number and trafficking. Mice were infected with A. phagocytophilum. Lineage-cKit+ HSPCs were enumerated and proliferation determined. CXCL12 and CXCR4 mRNA were quantified along with CXCL12 protein...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282207</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282207</guid>        </item>
        <item>
            <title>Biophysical investigations into the interactions of endotoxins with bile acids.</title>
            <link>http://www.medworm.com/index.php?rid=5282208&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21954318%26dopt%3DAbstract</link>
            <description>Authors: Fukuoka S, Richter W, Howe J, AndrÃ¤ J, RÃ¶ssle M, Alexander C, Gutsmann T, Brandenburg K
    Abstract
    The interaction of selected endotoxin preparations (lipid A from Erwinia carotovora and LPS Re and Ra from Salmonella enterica sv. Minnesota strains R595 and R60, respectively) with selected bile acids was investigated biophysically. Endotoxin aggregates were analyzed for their gel-to-liquid crystalline phase behavior, the type of their aggregates, the conformation of particular functional groups, and their Zeta potential in the absence and presence of the bile acids by applying Fourier-transform infrared spectroscopy, differential scanning calorimetry, measurements of the electrophoretic mobility, and synchrotron radiation X-ray scattering. In addition, the ability of the en...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282208</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282208</guid>        </item>
        <item>
            <title>Inhibitory effect of 10-hydroxy-trans-2-decenoic acid on LPS-induced IL-6 production via reducing I{kappa}B-{zeta} expression.</title>
            <link>http://www.medworm.com/index.php?rid=5282209&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21948282%26dopt%3DAbstract</link>
            <description>Authors: Sugiyama T, Takahashi K, Tokoro S, Gotou T, Neri P, Mori H
    Abstract
    The effect of 10-hydroxy-trans-2-decenoic acid (10H2DA), a major fatty acid component of royal jelly, was investigated on LPS-induced cytokine production in murine macrophage cell line, RAW264 cells. 10H2DA inhibited LPS-induced IL-6 production dose-dependently, but did not inhibit TNF-Î± production. 10H2DA inhibited LPS-induced NF-ÎºB activation in a dose-dependent fashion. In addition, NF-ÎºB activation induced by over-expression of either MyD88 or Toll/IL-1 receptor domain-containing adaptor inducing IFN-Î² (TRIF) was also inhibited by 10H2DA. Degradation of IÎºB-Î± and phosphorylation of IÎºB kinase-Î± were not inhibited by 10H2DA. On the other hand, reduction of LPS-induced IÎºB-Î¶ expression was disc...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282209</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282209</guid>        </item>
        <item>
            <title>Tetherin has negligible activity in restricting hepatitis C virus in hepatocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5282211&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21940748%26dopt%3DAbstract</link>
            <description>Authors: Ye L, Wang X, Li J, Liu J, Ramirez SH, Wu J, Ho W
    Abstract
    We investigated the ability of tetherin, a recently identified antiviral factor, in restricting hepatitis C virus (HCV) in the Japanese fulminant hepatitis-1 (JFH-1) infectious cell culture system. Human hepatocytes (Huh7, Huh7.5.1) expressedlow levels of endogenous tetherin, which could be induced by IFN-Î±. However, tetherin contributes little to IFN-Î±-mediated anti-HCV JFH-1 activity. Although tetherin could inhibit Vpu-deleted HIV-1 release, it had negligible activity in restricting HCV JFH-1 release from hepatocytes, which was evidenced by unaffected levels of intracellular/extracellular HCV RNA and infectious virus. The failure of tetherin's anti-HCV activity could not be related to the counteraction of HCV,...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282211</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282211</guid>        </item>
        <item>
            <title>Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=5247811&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926162%26dopt%3DAbstract</link>
            <description>In this study, we used a murine model of macrophage infection to demonstrate that H. pylori inhibits LPS-induced expression of iNOS and production of NO by macrophages. Suppression of LPS-induced NO production by macrophages led to elevated survival of H. pylori in a trans-well system. This effect was abrogated in macrophages from iNOS(-/-) mice. Analysis of iNOS mRNA and protein levels revealed that H. pylori inhibits iNOS expression at both transcriptional and post-transcriptional levels, and that these effects occurred with live bacteria. Furthermore, the effect of H. pylori involved down-regulation of the mitogen-activated protein kinase pathway and the translocation of active NF-ÎºB into the nucleus. Taken together, our results reveal a new mechanism by which H. pylori modulates the i...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247811</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247811</guid>        </item>
        <item>
            <title>Induction of decreased fecundity by tetanus toxoid hyper-immunization in C57BL/6 mice depends on the applied adjuvant.</title>
            <link>http://www.medworm.com/index.php?rid=5247810&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926163%26dopt%3DAbstract</link>
            <description>In this study we have investigated reproductive pathology induced in C57BL/6 mice by TTd hyper-immunization using a combination of different pretreatments (complete Freund's adjuvant or glycerol) and adjuvants (alhydrogel or glycerol). A decrease in fecundity was recorded in only C57BL/6 mice immunized with alhydrogel adjuvant, irrespective of the kind of applied pretreatment; it was associated with an increase in abundance of low affinity anti-Î²(2)GPI IgG antibodies and Th1 prevalence.
    PMID: 21926163 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247810</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247810</guid>        </item>
        <item>
            <title>Lipopolysaccharide infusion up-regulates hepcidin mRNA expression in equine liver.</title>
            <link>http://www.medworm.com/index.php?rid=5247809&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926164%26dopt%3DAbstract</link>
            <description>In this study, hepcidin gene expression was determined in the liver and bone marrow of six healthy horses after iv infusion of Escherichia coli O55:B5 LPS. The IL-6 gene expression was also determined in liver and bone marrow samples. Clinical and laboratory evaluations were measured at multiple time points between 0 and 240 h post-LPS infusion (PI). Liver and bone marrow biopsies were taken immediately before (baseline) and at 6 and 18 h PI. In response to endotoxin infusion, all horses showed characteristic clinical signs of endotoxemia. Plasma iron concentration was decreased significantly from the pre-infusion level at 8 h PI. Hypoferremia peak was observed at 12 h and returned to normal levels at 30 h PI. Relative real-time RT-PCR analysis showed that liver hepcidin and IL-6 mRNA expr...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247809</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247809</guid>        </item>
        <item>
            <title>Apoptosis induced by avian H5N1 virus in human monocyte-derived macrophages involves TRAIL-inducing caspase-10 activation.</title>
            <link>http://www.medworm.com/index.php?rid=5219596&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911414%26dopt%3DAbstract</link>
            <description>Authors: Ekchariyawat P, Thitithanyanont A, Sirisinha S, Utaisincharoen P
    Abstract
    Avian influenza virus H5N1 is a potentially fatal disease not only in birds, but also in humans. The virus is able to induce apoptosis in many cell types including macrophages and dendritic cells. In the present study, we demonstrated that TNF-related apoptosis-inducing ligand (TRAIL) is involved in apoptosis-associated mechanisms of apoptosis downstream of the TRAIL receptor in H5N1 virus-infected human monocyte-derived macrophages (MDMs). Activation of caspase-10 was also observed in avian virus H5N1-infected MDMs. In the presence of caspase-10 inhibitor, Z-AEVD-FMK, the activation of Bid and a release of apoptotic-inducing factor (AIF) from mitochondria were markedly reduced, resulting in a signif...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219596</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5219596</guid>        </item>
        <item>
            <title>A novel post-exposure medical countermeasure L-97-1 improves survival and acute lung injury following intratracheal infection with Yersinia pestis.</title>
            <link>http://www.medworm.com/index.php?rid=5157685&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21862597%26dopt%3DAbstract</link>
            <description>In this study, rats were infected intratracheally with viable Y. pestis [CO99 (pCD1( + )/Î”pgm) 1 Ã— 10( 8 ) CFU/animal] and treated daily for 3 d with ciprofloxacin (cipro), the A(1)AR antagonist L-97-1, or cipro plus L-97-1 starting at 0, 6, 24, 48, or 72 h post-Y. pestis. At 72 h post-Y. pestis, cipro plus L-97-1 significantly improved 6-d survival to 60-70% vs 28% for cipro plus H(2)O and 33% for untreated Y. pestis controls (P = 0.02, logrank test). Lung edema, hemorrhage and leukocyte infiltration index (LII) were evaluated histologically to produce ALI scores. Cipro plus L-97-1 significantly reduced lung edema, as well as aggregate lung injury scores vs controls or cipro plus H(2)O, and LII vs controls (P &amp;lt; 0.05, Student's unpaired t test). These results support efficacy for L-97...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157685</comments>
            <pubDate>Mon, 22 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157685</guid>        </item>
        <item>
            <title>Development of an electrochemical Limulus amebocyte lysate assay technique for portable and highly sensitive endotoxin sensor.</title>
            <link>http://www.medworm.com/index.php?rid=5141979&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21844129%26dopt%3DAbstract</link>
            <description>Authors: Inoue KY, Takahashi S, Ino K, Shiku H, Matsue T
    Abstract
    Here, we report the development of an electrochemical detection method for endotoxin based on the Limulus amebocyte lysate (LAL) assay. A mixture of LAL reagent and endotoxin sample solution was incubated for 1 h. The endotoxin activated a cascade reaction of zymogens contained in the LAL to generate p-nitroaniline (pNA) which was then electrochemically detected by differential pulse voltammetry (DPV). The generated pNA gave a clear peak at -0.75 V vs. silver/silver chloride (Ag/AgCl), which increased with the concentration of endotoxin in the LAL assay solution. This DPV detection was performed using an electrode chip device fabricated from a diamond-like carbon-coated glass substrate. This chip device could detect ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141979</comments>
            <pubDate>Sun, 14 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141979</guid>        </item>
        <item>
            <title>Immunization with an anti-idiotypic antibody against the broadly lipopolysaccharide-reactive antibody WN1 222-5 induces Escherichia coli R3-core-type specific antibodies in rabbits.</title>
            <link>http://www.medworm.com/index.php?rid=5141978&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21844130%26dopt%3DAbstract</link>
            <description>We describe the generation of a novel anti-idiotypic antibody that can induce LPS core-reactive antibodies upon immunization in rabbits and show that it is possible, in principle, to obtain LPS neutralizing antibodies by anti-idiotypic immunization against the mAb WN1 222-5. The mimicked epitope likely shares common determinants with the WN1 222-5 epitope, yet differences with respect to either affinity or specificity do exist, as binding to smaller oligosaccharides of the inner core was not observed.
    PMID: 21844130 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5141978</comments>
            <pubDate>Sun, 14 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5141978</guid>        </item>
        <item>
            <title>A new experimental murine model for lipopolysaccharide-mediated lethal shock with lung injury.</title>
            <link>http://www.medworm.com/index.php?rid=5106246&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21803777%26dopt%3DAbstract</link>
            <description>Authors: Takashi Y
    We have recently established a new experimental murine model for lipopolysaccharide (LPS)-mediated lethal shock with lung-specific injury. Severe lung injury is induced by administration of LPS into Î±-galactosylceramide (Î±-GalCer)-sensitized mice; the mice died with acute lung injury and respiratory distress within 24 h. Î±-GalCer activates natural killer T (NKT) cells in the lungs and liver, and induces the production of interferon (IFN)-Î³. However, IFN-Î³ signaling is only triggered in the lungs and makes them susceptible to LPS. On the other hand, IFN-Î³ signaling is inhibited in liver and results in few hepatic lesions. Unlike liver NKT cells, lung NKT cells fail to produce interleukin (IL)-4, which downregulates the IFN-Î³ signaling, in response to Î±-GalCer....</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106246</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5106246</guid>        </item>
        <item>
            <title>Phenotypic and functional profiles of CRIg (Z39Ig)-expressing macrophages in the large intestine.</title>
            <link>http://www.medworm.com/index.php?rid=5058844&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21768202%26dopt%3DAbstract</link>
            <description>This study will shed new light on opsonization and phagocytosis by large intestinal M.
    PMID: 21768202 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058844</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058844</guid>        </item>
        <item>
            <title>Inflammation-induced up-regulation of TLR2 expression in human endothelial cells is independent of differential methylation in the TLR2 promoter CpG island.</title>
            <link>http://www.medworm.com/index.php?rid=5058843&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21768203%26dopt%3DAbstract</link>
            <description>We examined the TLR2 promoter methylation pattern in resting HUVECs and compared it to cells treated either with the inflammatory cytokine TNF-Î± or the DNAdemethylating agent 5-azacytidine. DNA bisulfite conversion was followed by either genomic sequencing or single nucleotide primer extension (SNuPE) HPLC. Results of both techniques showed a low- or non-methylated TLR2 promoter in resting HUVECs and no alteration of the methylation pattern under inflammatory conditions. Whereas 5-azacytidine significantly increased the mRNA expression of the epigenetically regulated gene H19, TLR2 expression was not affected. Taken together, employing different methodological approaches, our data show no implication of methylation pattern changes in inflammatory induction of TLR2 expression in human endo...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058843</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058843</guid>        </item>
        <item>
            <title>Sindbis virus induced phosphorylation of IRF3 in human embryonic kidney cells is not dependent on mTOR.</title>
            <link>http://www.medworm.com/index.php?rid=5058842&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21768204%26dopt%3DAbstract</link>
            <description>Authors: Dhanushkodi NR, Mohankumar V, Raju R
    The mammalian target of rapamycin (mTOR) plays critical roles in immunity. We previously showed that infection of human embryonic kidney (HEK) cells with Sindbis virus (SIN), an enveloped RNA alphavirus, profoundly suppresses Akt/mTOR signaling, and host translation late during infection. To understand how SIN mediated suppression of mTOR affects innate response, we analyzed phosphorylation of interferon regulatory factor 3 (IRF3) and expression of two antiviral genes. Here we show strong phosphorylation of IRF3, and an increase in mRNA levels for antiviral genes interferon stimulated gene (ISG)56 and interferon gamma inducible protein (IP)-10 when intracellular viral RNA levels are high during late infection. The mTOR inhibitors rapamycin ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5058842</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5058842</guid>        </item>
        <item>
            <title>Rotavirus-induced IFN-{beta} promotes anti-viral signaling and apoptosis that modulate viral replication in intestinal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5011322&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21733977%26dopt%3DAbstract</link>
            <description>Authors: Frias AH, Jones RM, Fifadara NH, Vijay-Kumar M, Gewirtz AT
    Rotavirus (RV), a leading cause of diarrhea, primarily infects intestinal epithelial cells (IEC). Rotavirus-infected IEC produce IFN-Î² and express hundreds of IFN-dependent genes. We thus hypothesized that type 1 IFN plays a key role in helping IEC limit RV replication and/or protect against cell death. To test this hypothesis, we examined IEC (HT29 cells) infected with RV (MOI 1) Â± neutralizing antibodies to IFN-Î±/Î² via microscopy and SDS-PAGE immunoblotting. We hypothesized that neutralization of IFN would be clearly detrimental to RV-infected IEC. Rather, we observed that blockade of IFN function rescued IEC from the apoptotic cell death that otherwise would have occurred 24-48 h following exposure to RV. This r...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5011322</comments>
            <pubDate>Tue, 05 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5011322</guid>        </item>
        <item>
            <title>Induction of triggering receptor expressed on myeloid cells (TREM-1) in airway epithelial cells by 1,25(OH)2 vitamin D3.</title>
            <link>http://www.medworm.com/index.php?rid=4963142&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21690199%26dopt%3DAbstract</link>
            <description>Authors: Rigo I, McMahon L, Dhawan P, Christakos S, Yim S, Ryan LK, Diamond G
    The airway epithelium plays a role in host defense through the binding of innate immune receptors, which leads to the activation of inflammatory mediators, including antimicrobial peptides. The active form of vitamin D, 1,25(OH)(2)D(3), induces the expression of the antimicrobial peptide LL-37 in both myeloid cells and airway epithelial cells (AEC). Here, we demonstrate that mRNA encoding triggering receptor expressed on myeloid cells (TREM)-1 was induced up to 12-fold by 1,25(OH)(2)D(3) in normal human bronchial epithelial (NHBE) cells and in well-differentiated cultures of six airway epithelial cell lines from patients with cystic fibrosis and healthy individuals. TREM-2 and DAP12 were also expressed in air...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4963142</comments>
            <pubDate>Sun, 19 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4963142</guid>        </item>
        <item>
            <title>Nuclear factor-kB mediated lipopolysaccharide-induced mRNA expression of hepcidin in human peripheral blood leukocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4963144&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21685415%26dopt%3DAbstract</link>
            <description>In this study, we explored the expression and signaling mechanism regulating hepcidin mRNA expression in peripheral blood leukocytes. The mRNA levels of hepcidin in peripheral blood leukocytes from patients with severe sepsis (n = 14) was significantly higher than those in healthy controls (n = 16;0.286 Â± 0.065 vs 0.068 Â± 0.025; P &amp;lt; 0.05). Ex vivo studies found hepcidin mRNA can be highly induced by challenge of 100 ng/ml LPS or 20 ng/ml TNF-Î± in peripheral blood leukocytes rather than IL-6, IL-1 and IFN-Î³. Anti-TNF-Î± antibody significantly decreased the levels of hepcidin mRNA induced by LPS. Inhibitor of nuclear factor (NF)-ÎºB rather than that of STAT3 completely abolished the inducibility of hepcidin mRNA in PBMCs and neutrophils. These results indicate that hepcidin mRNA expre...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4963144</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4963144</guid>        </item>
        <item>
            <title>Effects of catecholamines on hepatic and skeletal muscle mitochondrial respiration after prolonged exposure to faecal peritonitis in pigs.</title>
            <link>http://www.medworm.com/index.php?rid=4815848&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21525237%26dopt%3DAbstract</link>
            <description>Authors: Vuda M, Brander L, SchrÃ¶eder R, Jakob SM, Takala J, Djafarzadeh S
    Use of norepinephrine to increase blood pressure in septic animals has been associated with increased efficiency of hepatic mitochondrial respiration. The aim of this study was to evaluate whether the same effect could be reproduced in isolated hepatic mitochondria after prolonged in vivo exposure to faecal peritonitis. Eighteen pigs were randomized to 27 h of faecal peritonitis and to a control condition (n = 9 each group). At the end, hepatic mitochondria were isolated and incubated for one hour with either norepinephrine or placebo, with and without pretreatment with the specific receptor antagonists prazosin and yohimbine. Mitochondrial state 3 and state 4 respiration were measured for respiratory chain com...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4815848</comments>
            <pubDate>Tue, 26 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4815848</guid>        </item>
        <item>
            <title>Complement and non-complement activating functions of C1q: A prototypical innate immune molecule.</title>
            <link>http://www.medworm.com/index.php?rid=4710795&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21450789%26dopt%3DAbstract</link>
            <description>Authors: Nayak A, Pedenekar L, Reid KB, Kishore U
    C1q is a versatile innate immune molecule that serves as the initiation subcomponent of the classical complement pathway. In addition, it is also a potent pattern recognition molecule, the versatility of which has fuelled its functional flexibility. C1q recognises an array of self, non-self and altered-self ligands. The broad-spectrum ligand-binding potential of C1q is facilitated by the modular organisation of the heterotrimeric globular head region, its ability to change its conformation in a very subtle way, and the manner in which this ancient molecule appears to have evolved to deal with the different types of ligands. Over recent years, molecules that resemble C1q have been put together to form the C1q family. In this review, we b...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4710795</comments>
            <pubDate>Tue, 29 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4710795</guid>        </item>
        <item>
            <title>Inflammation inhibits the expression of phosphoenolpyruvate carboxykinase in liver and adipose tissue.</title>
            <link>http://www.medworm.com/index.php?rid=4710794&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21450790%26dopt%3DAbstract</link>
            <description>Authors: Feingold KR, Moser A, Shigenaga JK, Grunfeld C
    Inhibition of adipocyte triglyceride biosynthesis is required for fatty acid mobilization during inflammation. Triglyceride biosynthesis requires glycerol 3-phosphate and phosphoenolpyruvate carboxykinase (PEPCK) plays a key role. We demonstrate that LPS, zymosan, and TNF-Î± decrease PEPCK in liver and fat. Turpentine decreases PEPCK in liver, but not in fat. The LPS-induced decrease in PEPCK does not occur in TLR4 deficient animals, indicating that this receptor is required. The LPS-induced decrease in hepatic PEPCK does not occur in TNF receptor/IL-1 receptor knockout mice, but occurs in fat, indicating that TNF-Î±/IL-1 is essential for the decrease in liver but not fat. In 3T3-L1 adipocytes TNF-Î±, IL-1, IL-6, and IFNÎ³ inhibit...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4710794</comments>
            <pubDate>Tue, 29 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4710794</guid>        </item>
        <item>
            <title>Anti-inflammatory modulation of immune response by probiotic Escherichia coli Nissle 1917 in human blood mononuclear cells.</title>
            <link>http://www.medworm.com/index.php?rid=4593175&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21382908%26dopt%3DAbstract</link>
            <description>Authors: GÃ¼ttsches AK, LÃ¶seke S, ZÃ¤hringer U, Sonnenborn U, Enders C, Gatermann S, Bufe A
    Escherichia coli Nissle 1917 (EcN) bears a defect in its LPS biosynthesis leading to truncated variable oligosaccharide-antigen chains and a semi-rough phenotype. It is effectively inactivated by complement factors due to resolved serum resistance and is, therefore, safe as a probiotic strain, i.e. for the treatment of inflammatory gastrointestinal diseases. It is unknown whether the modification of LPS in EcN contributes to its probiotic properties. Purified LPS from EcN and wild-type LPS from uropathogenic E. coli W536 together with raw lysates of both strains were analyzed for their gene expression activity with human PBMCs measured by microarrays. Comparing the two LPS molecules and the two...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593175</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593175</guid>        </item>
        <item>
            <title>Deactivation of the lipopolysaccharide antagonist eritoran (E5564) by high-density lipoprotein-associated apolipoproteins.</title>
            <link>http://www.medworm.com/index.php?rid=4593174&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21382909%26dopt%3DAbstract</link>
            <description>Authors: Fleischer JG, Rossignol D, Francis GA, Chan T, Lynn M, Wasan KM
    Lipid A, the active moiety of LPS, exerts its effects through interaction with TLR4, triggering a signalling cascade that results in the release of pro-inflammatory cytokines. Eritoran is a lipid A analogue that competes with LPS for binding to TLR4; however, after intravenous administration, it undergoes a time-dependent deactivation as a consequence of binding to high-density lipoproteins (HDLs). The site of eritoran association with HDL remains unknown. Therefore the aim of this study was to determine if HDL-associated apolipoproteins A1, A2, serum amyloid A (SAA) and C1, inhibit the ability of eritoran to block LPS-induced TNF-Î± release from whole blood. Eritoran activity after LPS stimulation in human whole ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593174</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593174</guid>        </item>
        <item>
            <title>In memoriam.</title>
            <link>http://www.medworm.com/index.php?rid=4481018&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21300816%26dopt%3DAbstract</link>
            <description>Authors: Holst O
    
    PMID: 21300816 [PubMed - in process] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481018</comments>
            <pubDate>Wed, 16 Feb 2011 02:15:03 +0100</pubDate>
            <guid isPermaLink="false">4481018</guid>        </item>
        <item>
            <title>Referees 2010.</title>
            <link>http://www.medworm.com/index.php?rid=4481017&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21300817%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 21300817 [PubMed - in process] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481017</comments>
            <pubDate>Wed, 16 Feb 2011 02:15:03 +0100</pubDate>
            <guid isPermaLink="false">4481017</guid>        </item>
        <item>
            <title>Mutational analysis of human NOD1 and NOD2 NACHT domains reveals different modes of activation.</title>
            <link>http://www.medworm.com/index.php?rid=4481016&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21310790%26dopt%3DAbstract</link>
            <description>Authors: Zurek B, Proell M, Wagner RN, Schwarzenbacher R, Kufer TA
    Nucleotide-binding oligomerization domain-containing protein (NOD)1 and NOD2 are intracellular pattern recognition receptors (PRRs) of the nucleotide-binding domain and leucine-rich repeat containing (NLR) gene family involved in innate immune responses. Their centrally located NACHT domain displays ATPase activity and is necessary for activation and oligomerization leading to inflammatory signaling responses. Mutations affecting key residues of the ATPase domain of NOD2 are linked to severe auto-inflammatory diseases, such as Blau syndrome and early-onset sarcoidosis. By mutational dissection of the ATPase domain function, we show that the NLR-specific extended Walker B box (DGhDE) can functionally replace the canonica...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481016</comments>
            <pubDate>Thu, 10 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4481016</guid>        </item>
        <item>
            <title>Low susceptibility of NC/Nga mice to the lipopolysaccharide-mediated lethality with D-galactosamine sensitization and the involvement of fewer natural killer T cells.</title>
            <link>http://www.medworm.com/index.php?rid=4222575&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21113080%26dopt%3DAbstract</link>
            <description>Authors: Koide N, Morikawa A, Odkhuu E, Haque A, Badamtseren B, Naiki Y, Komatsu T, Yoshida T, Yokochi T
    The LPS-mediated lethality of NC/Nga mice, having fewer NKT cells, was examined by using d-galactosamine (d-GalN)-sensitization. The NC/Nga mice were not killed by a simultaneous administration of d-GalN and LPS whereas all C57BL/6 (B6) control mice were killed. The injection of d-GalN and LPS failed to elevate the levels of serum alanine aminotransferase and caspase 3 in the liver tissues of NC/Nga mice. Further, the nitric oxide (NO) level of the d-GalN- and LPS-injected NC/Nga mice was much lower than those of the B6 mice. The expression of an inducible NO synthase (iNOS) was significantly reduced in the livers of NC/Nga mice. However, there was no significant difference in LPS-i...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4222575</comments>
            <pubDate>Fri, 26 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4222575</guid>        </item>
        <item>
            <title>Biphasic adaptative responses in VLDL metabolism and lipoprotein homeostasis during Gram-negative endotoxemia.</title>
            <link>http://www.medworm.com/index.php?rid=4222570&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21113081%26dopt%3DAbstract</link>
            <description>In conclusion, endotoxin challenge induces increases in plasma NEFA and large, triglyceride-rich VLDL. After approximately 12 h, the triglyceride-rich VLDLs are replaced by medium-sized, triglyceride-poor VLDL particles. Hepatic apoB mRNA abundance also increases during the second period, suggesting a role for apoB protein expression in the acute reaction against sepsis.
    PMID: 21113081 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4222570</comments>
            <pubDate>Fri, 26 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4222570</guid>        </item>
        <item>
            <title>Comparison of temperature rise interpretations in the rabbit pyrogen test among Chinese, Japanese, European, and United States pharmacopeias and 2-2-2 theoretical models proposed by S. Hoffmann.</title>
            <link>http://www.medworm.com/index.php?rid=4187442&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088045%26dopt%3DAbstract</link>
            <description>Authors: Du Y, Li XJ, Tan DJ
    Although the rabbit pyrogen test is one of the crucial methods included in each pharmacopeia to evaluate the safety of parenteral medicine, the experimental procedures and pyrogen result judgment algorithms (PRJAs) are still greatly different from one another. In the first stage of testing, original data of 879 batches from a total of 2637 rabbits in our laboratory were judged by PRJAs in the Chinese Pharmacopoeia 2005 III, the Japanese Pharmacopoeia XIV, the Japanese Pharmacopoeia XV, the European Pharmacopeia 6.0, the United States Pharmacopoeia 32 NF27 and two theoretical models proposed by S. Hoffmann, respectively. The results were analyzed to evaluate the effects of various PRJAs. It was shown that: (i) the significant differences in the results judge...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187442</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187442</guid>        </item>
        <item>
            <title>Immune alterations after selective rapid eye movement or total sleep deprivation in healthy male volunteers.</title>
            <link>http://www.medworm.com/index.php?rid=4187441&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088046%26dopt%3DAbstract</link>
            <description>Authors: Ruiz FS, Andersen ML, Martins RC, Zager A, Lopes JD, Tufik S
    We investigated the impact of two nights of total sleep deprivation (SD) or four nights of rapid eye movement (REM) SD on immunological parameters in healthy men. Thirty-two volunteers were randomly assigned to three protocols (control, total SD or REM SD). Both SD protocols were followed by three nights of sleep recovery. The control and REM SD groups had regular nights of sleep monitored by polysomnography. Circulating white blood cells (WBCs), T- (CD4/CD8) and B-lymphocytes, Ig classes, complement and cytokine levels were assessed daily. Two nights of total SD increased the numbers of leukocytes and neutrophils compared with baseline levels, and these levels returned to baseline after 24 h of sleep recovery. The C...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187441</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187441</guid>        </item>
        <item>
            <title>Both inflammatory and classical lipolytic pathways are involved in lipopolysaccharides-induced lipolysis in human adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4187440&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088047%26dopt%3DAbstract</link>
            <description>This study aims to unravel the cellular mechanisms leading to the lipopolysaccharide (LPS) effects in human adipocytes. Subcutaneous pre-adipocytes surgically isolated from patients were differentiated into mature adipocytes in vitro. Lipolysis was assessed by measurement of glycerol release and mRNA expression of pro-inflammatory cytokines were evaluated by real-time PCR. Treatment with LPS for 24 h induced a dose-dependent increase in interleukin (IL)-6 and IL-8 mRNA expression. At 1 Âµg/ml LPS, IL-6 and IL-8 were induced to 19.5 Â± 1.8-fold and 662.7 Â± 91.5-fold (P &amp;lt; 0.01 vs basal), respectively. From 100 ng/ml to 1 Âµg/ml, LPS-induced lipolysis increased to a plateau of 3.1-fold above basal level (P &amp;lt; 0.001 vs basal). Co-treatment with inhibitors of inhibitory kappa B kinase kin...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187440</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187440</guid>        </item>
        <item>
            <title>Ron receptor deficient alveolar myeloid cells exacerbate LPS-induced acute lung injury in the murine lung.</title>
            <link>http://www.medworm.com/index.php?rid=4187439&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088048%26dopt%3DAbstract</link>
            <description>In this study, we report that loss of Ron signaling selectively in myeloid cells results in increased lung injury following intranasal administration of LPS as measured by increases in TNF-Î± production, ensuing neutrophil accumulation and increased lung histopathology. These findings corroborate the role of Ron receptor tyrosine kinase as a negative regulator of inflammation and further demonstrate the in vivo significance of Ron signaling selectively in myeloid cells as a major regulator of this response in vivo. These data authenticate Ron as a potential target in innate immunity and TNF-Î±-mediated pathologies.
    PMID: 21088048 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187439</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187439</guid>        </item>
        <item>
            <title>Association of genetic variants of mannan-binding (MBL) lectin-2 gene, MBL levels and function in ulcerative colitis and Crohn's disease.</title>
            <link>http://www.medworm.com/index.php?rid=4187438&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088049%26dopt%3DAbstract</link>
            <description>In conclusion, single nucleotide polymorphism in the MBL-2 gene is an important risk factor significantly affecting MBL levels and function in the development of ulcerative colitis among Indians.
    PMID: 21088049 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187438</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187438</guid>        </item>
        <item>
            <title>CXC chemokine ligand 4 (CXCL4) down-regulates CC chemokine receptor expression on human monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4187437&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088050%26dopt%3DAbstract</link>
            <description>In conclusion, CXCL4 may act as a selective regulator of monocyte migration by stimulating the release of autocrine, receptor-desensitizing chemokine ligands. Our results stress a co-ordinating role for CXCL4 in the cross-talk between platelets and monocytes during early inflammation.
    PMID: 21088050 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187437</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187437</guid>        </item>
        <item>
            <title>Nucleotide-binding oligomerization domain-containing protein 2 regulates suppressor of cytokine signaling 3 expression in Burkholderia pseudomallei- infected mouse macrophage cell line RAW 264.7.</title>
            <link>http://www.medworm.com/index.php?rid=4187436&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088051%26dopt%3DAbstract</link>
            <description>Authors: Pudla M, Kananuruk A, Limposuwan K, Sirisinha S, Utaisincharoen P
    Burkholderia pseudomallei, a causative agent of melioidosis, is a facultative intracellular Gram-negative bacterium that can survive and multiply inside the macrophages. Toll-like receptors are one class of pattern recognition receptors (PRRs) that have been documented to play significant role in B. pseudomallei infection. In the present study, we investigated a potential role of nucleotide-binding oligomerization domain-containing protein 1 and 2 (NOD1 and NOD2), cytoplasmic pattern recognition receptors, in B. pseudomallei-infected mouse macrophage cell line RAW 264.7. Both live and heat-killed B. pseudomallei were able to up-regulate NOD1 and NOD2 expression in a time-dependent manner. Marked reduction of a n...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187436</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187436</guid>        </item>
        <item>
            <title>Neisseria meningitidis lipid A mutant LPSs function as LPS antagonists in humans by inhibiting TLR 4-dependent cytokine production.</title>
            <link>http://www.medworm.com/index.php?rid=4187435&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088052%26dopt%3DAbstract</link>
            <description>Authors: Sprong T, van der Ley P, Abdollahi-Roodsaz S, Joosten L, van der Meer J, Netea M, van Deuren M
    Lipopolysaccharide is a major constituent of the outer membrane of Gram-negative bacteria and important in the induction of pro-inflammatory responses. Recently, novel LPS species derived from Neisseria meningitidis H44/76 by insertional inactivation of the lpxL1 and lpxL2 genes have been created with a lipid A portion consisting of five (penta-acylated lpxL1) or four (tetra-acylated lpxL2) fatty acids connected to the glucosamine backbone instead of six fatty acids in the wild-type LPS. We show that these mutant LPS-types are poor inducers of cytokines (tumor-necrosis factor-Î±, IL-1Î², IL-10, IL-RA) in human mononuclear cells. Both penta- and tetra-acylated meningococcal LPSs were ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187435</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187435</guid>        </item>
        <item>
            <title>Editorial.</title>
            <link>http://www.medworm.com/index.php?rid=4000797&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20864550%26dopt%3DAbstract</link>
            <description>Authors: Holst O
    
    PMID: 20864550 [PubMed - in process] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4000797</comments>
            <pubDate>Sat, 25 Sep 2010 16:42:03 +0100</pubDate>
            <guid isPermaLink="false">4000797</guid>        </item>
        <item>
            <title>Method of bacterial killing differentially affects the human innate immune response to Staphylococcus epidermidis.</title>
            <link>http://www.medworm.com/index.php?rid=3934922&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20807722%26dopt%3DAbstract</link>
            <description>Conclusions: Killing of extracellular bacteria has significant qualitative and quantitative effects on key aspects of innate responses in vitro. Interpretation of in vitro data and extrapolation of findings should take into account the potential effects of bacterial preparation and should not assume that responses to killed bacteria are predictive of responses to live organisms.
    PMID: 20807722 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3934922</comments>
            <pubDate>Mon, 30 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3934922</guid>        </item>
        <item>
            <title>Obesity and immune cells in Saudi females.</title>
            <link>http://www.medworm.com/index.php?rid=3885988&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20699279%26dopt%3DAbstract</link>
            <description>In this study, the effect of obesity on the immune system of 119 Saudi female university students was investigated. Using a blood sample from each subject, the following immune-related parameters were determined: total and differential white blood cell counts (WBCs), total lymphocyte and sub-lymphocyte cell counts. Two measures of body fat were used: the body mass index (BMI) and the waist-to-hip ratio (WHR) to correlate body weight to the other measured parameters. A significant correlation was present between BMI and WHR each with total white blood cells, neutrophils, and CD4 lymphocyte concentrations. Some other parameters were only affected by the increase in the BMI but not the WHR, such as platelets, while others were affected by the WHR only, such as total T-cells. On the other hand...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3885988</comments>
            <pubDate>Mon, 09 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3885988</guid>        </item>
        <item>
            <title>Regulation of colon cancer cell proliferation and migration by MD-2 activity.</title>
            <link>http://www.medworm.com/index.php?rid=3885987&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20699280%26dopt%3DAbstract</link>
            <description>Authors: Grondin V, Seksik P, Dumont S, Thomas G, Trugnan G, FlÃƒÂ©jou JF, Masliah J, Wendum D, Bachelet M
    Evidence suggests that signalling through lipopolysaccharide (LPS) has a significant role in the development of gastrointestinal malignancies. We previously demonstrated the critical role of myeloid differentiation (MD)-2, the essential co-receptor of LPS, for induction of cyclooxygenase (Cox)-2 in intestinal epithelial cells. Cyclooxigenase-2 was suggested to play a key role in colorectal cancer through the effects of prostaglandin (PG) E2 generated. We, therefore, addressed the role of MD-2 in several parameters related to malignancy, namely cell proliferation and migration, using colon cancer cells (HT-29). We found that overexpression of MD-2 confers a significantly greater pr...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3885987</comments>
            <pubDate>Mon, 09 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3885987</guid>        </item>
        <item>
            <title>MyD88-dependent pro-inflammatory cytokine response contributes to lethal toxicity of staphylococcal enterotoxin B in mice.</title>
            <link>http://www.medworm.com/index.php?rid=3885986&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20699281%26dopt%3DAbstract</link>
            <description>We examined the role of the signaling adaptor MyD88 in cell culture and in a mouse model of toxic shock. Our results indicated that elevated tumor necrosis factor-alpha, interferon-gamma, interleukin (IL)-1alpha/beta and IL-6 production from mouse spleen cells treated with SEB alone or in combination with lipopolysaccharide (LPS) was regulated by MyD88. Elevated levels of MyD88 protein in spleen cells, as well as in CD11c(+) or Mac3(+) cells, and activation of nuclear factor-kappaB in spleen cells were observed in mice treated with SEB. An SEB-dose dependent lethality was observed in LPS-potentiated and in D-galactosamine-sensitized mice. D-Galactosamine treatment of spleen cells had no effect in cytokine induction but rather increased the sensitivity to toxic shock in mice. Our results de...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3885986</comments>
            <pubDate>Mon, 09 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3885986</guid>        </item>
        <item>
            <title>The many faces of the YopM effector from plague causative bacterium Yersinia pestis and its implications for host immune modulation.</title>
            <link>http://www.medworm.com/index.php?rid=3885985&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20699282%26dopt%3DAbstract</link>
            <description>Authors: Soundararajan V, Patel N, Subramanian V, Sasisekharan V, Sasisekharan R
    The Yersinia outer protein (Yop) M effector from the Yersinia pestis bacterium is well-known for being a critical virulence determinant; however, structural insight vis-ÃƒÂ -vis its role in Y. pestis pathogenesis has been elusive. Here, we investigate the intact sequence of the YopM protein through our recently developed fold identification and homology modeling tools, and analyze the immune modulatory potential of its constituent domains. We identify a putative novel E3 ligase (NEL) domain towards the C-terminal tail of YopM and characterize its active site, to show that YopM could function as an autoregulated bacterial type E3 ubiquitin ligase. We further identify unreported NEL domains in several other ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3885985</comments>
            <pubDate>Mon, 09 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3885985</guid>        </item>
        <item>
            <title>Arsenic trioxide reduces 2,4,6-trinitrobenzene sulfonic acid-induced murine colitis via nuclear factor-{kappa}B down-regulation and caspase-3 activation.</title>
            <link>http://www.medworm.com/index.php?rid=3855845&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20693187%26dopt%3DAbstract</link>
            <description>Authors: Singer M, Trugnan G, Chelbi-Alix MK
    Arsenic trioxide, As2O3, already used in human anti-cancer therapy, is also an efficient agent against the autoimmune and inflammatory diseases developed in MRL/lpr mice. Inflammatory bowel diseases (IBDs), notably Crohn's disease, which remain without efficient treatment, display autoimmune and inflammatory components. We, therefore, hypothesized that As2O3 may be active on IBDs. Using the 2,4,6-trinitrobenzene sulfonic acid-induced murine model of colitis, we demonstrate that As2O3 used either in a preventive or a curative mode markedly reduced the induced colitis as assessed by macroscopic and microscopic scores, leading to prolonged mice survival. In addition, As2O3 was able to inhibit NF-kappaB expression and DNA-binding in colon extrac...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3855845</comments>
            <pubDate>Thu, 05 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3855845</guid>        </item>
        <item>
            <title>Defined particle ligands trigger specific defense mechanisms of macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=3827416&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682584%26dopt%3DAbstract</link>
            <description>Authors: Dykstra T, Utermoehlen O, Haas A
    Phagocytosis is a receptor-mediated process for sequestration and inactivation of infectious microbes. It can be triggered by microbial surface compounds or particle-attached host proteins. We monitored the effector functions of murine bone marrow-derived macrophages (BMMs) in response to polystyrene-streptavidin beads coated with the defined ligands IgG1, beta-glucan, mannan, complement factors C1q or iC3b, or fibronectin (FN). Cell-autonomous effector mechanisms (uptake, phagosome maturation, cytokine responses and killing activity) were differentially triggered. All particle-ligand complexes stimulated the release of nitric oxide, but only beads coated with IgG, complement factors or FN caused production of superoxide. Beads coated with C1q,...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827416</comments>
            <pubDate>Mon, 02 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827416</guid>        </item>
        <item>
            <title>Role of calcium in lipopolysaccharide-induced calcitonin gene expression in human adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3827415&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682585%26dopt%3DAbstract</link>
            <description>Authors: Radimerski TM, Grisouard J, Timper K, Zulewski H, Christ-Crain M, Keller U, MÃƒÂ¼ller B
    Severe systemic infections induce ubiquitous calcitonin (CALC) gene expression with release of calcitonin peptides, namely procalcitonin, calcitonin gene-related peptide and adrenomedullin. Using an in vitro model for bacterial infection, we tested the hypothesis that intracellular calcium concentration ([Ca(2+)]i) is elevated after lipopolysaccharide (LPS) stimulation and is responsible for the LPS-mediated increase in CALC gene expression and protein secretion. In our human adipocyte model, LPS did not show any cytotoxic effects and induced increased CALC-I gene mRNA expression. Additionally, LPS provoked an elevation in [Ca(2+)]i. The LPS-induced increase in CALC-I gene mRNA was partiall...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827415</comments>
            <pubDate>Mon, 02 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827415</guid>        </item>
        <item>
            <title>Mitogen-activated protein kinases p38 and ERK1/2 regulated control of Mycobacterium avium replication in primary murine macrophages is independent of tumor necrosis factor-alpha and interleukin-10.</title>
            <link>http://www.medworm.com/index.php?rid=3827414&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682586%26dopt%3DAbstract</link>
            <description>Authors: Klug K, Ehlers S, Uhlig S, Reiling N
    In macrophages, mitogen-activated protein kinases (MAPK) are critical regulators of both, mycobacterial replication and mycobacteria-induced cytokine formation. To segregate direct effects of MAPK function on mycobacterial replication from indirect, cytokine-mediated effects, we studied the growth of Mycobacterium avium strains in wild-type and tumor necrosis factor (TNF)-alpha- or interleukin (IL)-10-deficient bone marrow-derived murine macrophages. Using specific inhibitors of the p38- and the ERK1/2-MAPK pathways, we found that the use of SB203580 always reduced, whereas the presence of PD98059 always promoted, bacterial replication of highly virulent and intermediately virulent M. avium strains, independent of endogenous TNF-alpha or IL...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827414</comments>
            <pubDate>Mon, 02 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827414</guid>        </item>
        <item>
            <title>Activation of cytokine-producing and antitumor activities of natural killer cells and macrophages by engagement of Toll-like and NOD-like receptors.</title>
            <link>http://www.medworm.com/index.php?rid=3827413&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682587%26dopt%3DAbstract</link>
            <description>In this study, we examined the capacities of expressed TLRs and NLRs to elicit cytokine production in human NK cells and THP1 macrophages, and to activate NK cytotoxicity against the squamous cell carcinoma of head and neck cell line Tu167 and erythroleukemia K562 cells. We found that NK cells express high levels of NOD2, NLRP3, TLR3, TLR7, and TLR9, while NOD1 was expressed at low levels. All tested NLR and TLR agonists potentiated NK cytotoxicity against Tu167 cells, whereas only poly (I:C) increased NK cytotoxicity against K562 cells. Poly (I:C) and Escherichia coli RNA markedly up-regulated TNF-alpha and IFN-gamma expression in the NK92 cell line and human CD56(+)CD3(-;) primary NK cells. High levels of NOD2, TLR7 and TLR9 proteins were observed in human THP1 cells, followed by TLR3, N...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827413</comments>
            <pubDate>Mon, 02 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827413</guid>        </item>
        <item>
            <title>Morphology, size distribution, and aggregate structure of lipopolysaccharide and lipid A dispersions from enterobacterial origin.</title>
            <link>http://www.medworm.com/index.php?rid=3827412&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682588%26dopt%3DAbstract</link>
            <description>Authors: Richter W, Vogel V, Howe J, Steiniger F, Brauser A, Koch MH, Roessle M, Gutsmann T, Garidel P, MÃƒÂ¤ntele W, Brandenburg K
    Lipopolysaccharides (LPSs) from Gram-negative bacteria are strong elicitors of the human immune systems. There is strong evidence that aggregates and not monomers of LPS play a decisive role at least in the initial stages of cell activation of immune cells such as mononuclear cells. In previous reports, it was shown that the biologically most active part of enterobacterial LPS, hexa-acyl bisphosphorylated lipid A, adopts a particular supramolecular conformation, a cubic aggregate structure. However, little is known about the size and morphology of these aggregates, regarding the fact that LPS may have strong variations in the length of the saccharide chain...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827412</comments>
            <pubDate>Mon, 02 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827412</guid>        </item>
        <item>
            <title>Distinct regulation by lipopolysaccharides of the expression of interleukin-1{beta} by murine macrophages and salivary glands.</title>
            <link>http://www.medworm.com/index.php?rid=3827411&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682589%26dopt%3DAbstract</link>
            <description>In conclusion, IL-1beta is constitutively expressed by submandibular glands and its secretion is not regulated by a P2X7 agonist. In these cells, LPS do not activate the nuclear factor-kappaB-pro-IL-1beta axis in spite of the expression of the proteins involved in their recognition.
    PMID: 20682589 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827411</comments>
            <pubDate>Mon, 02 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827411</guid>        </item>
        <item>
            <title>Temperament influences endotoxin-induced changes in rectal temperature, sickness behavior, and plasma epinephrine concentrations in bulls.</title>
            <link>http://www.medworm.com/index.php?rid=3827410&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20682590%26dopt%3DAbstract</link>
            <description>This study was designed to determine the influence of temperament on endotoxin-induced changes in body temperature, sickness behavior, and stress hormone concentrations in cattle. Brahman bulls were selected based on temperament score measured 28 d prior to weaning. In dwelling recording devices were used to monitor rectal temperature, and jugular catheters were used to collect blood samples to determine cortisol and epinephrine concentrations before and after LPS administration (0.5 microg/kg body weight). Temperamental bulls had the lowest peak rectal temperature and sickness behavior scores relative to the Calm and Intermediate bulls. Prior to the administration of LPS, Temperamental bulls had greater cortisol and epinephrine concentrations than Calm or Intermediate bulls. Cortisol conc...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3827410</comments>
            <pubDate>Mon, 02 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3827410</guid>        </item>
        <item>
            <title>Inducible expression of human {beta}-defensin 2 by Chlamydophila pneumoniae in brain capillary endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3780605&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20647256%26dopt%3DAbstract</link>
            <description>Authors: Tiszlavicz Z, EndrÃƒÂ©sz V, NÃƒÂ©meth B, Megyeri K, Orosz L, SeprÃƒÂ©nyi G, MÃƒÂ¡ndi Y
    Defensins are an important family of natural antimicrobial peptides. Chlamydophila pneumoniae, a common cause of acute respiratory infection, has a tendency to cause persistent inflammatory diseases such as atherosclerosis, which may lead to cardiovascular disease or stroke. As endothelial cells are related to the physiopathology of stroke, the effects of in vitro C. pneumoniae infection on the expression of human beta-defensin 2 (HBD-2) in brain capillary endothelial cells (BB19) was investigated. A time-dependent increase in HBD-2 mRNA was observed by means of real-time reverse transcription PCR (RT-PCR) in BB19 cells following C. pneumoniae infection, with a maximum increase at 24 h. A gr...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3780605</comments>
            <pubDate>Mon, 19 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3780605</guid>        </item>
        <item>
            <title>Antibody equivalent molecules of the innate immune system: parallels between innate and adaptive immune proteins.</title>
            <link>http://www.medworm.com/index.php?rid=3656190&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20529970%26dopt%3DAbstract</link>
            <description>Authors: Palaniyar N
    Soluble pattern-recognition innate immune proteins functionally resemble the antibodies of the adaptive immune system. Two major families of such proteins are ficolins and collectins or collagenous lectins (e.g. mannose-binding lectin [MBL], surfactant proteins [SP-A and SP-D] and conglutinin). In general, subunits of ficolins and collectins recognize the carbohydrate arrays of their targets via globular trimeric carbohydrate-recognition domains (CRDs) whereas IgG, IgM and other antibody isotypes recognize proteins via dimeric antigen-binding domains (Fab). Considering the structure and functions of these proteins, ficolins and MBL are analogous to molecules with the complement activating functions of C1q and the target recognition ability of IgG. Although the stru...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3656190</comments>
            <pubDate>Sun, 13 Jun 2010 05:09:02 +0100</pubDate>
            <guid isPermaLink="false">3656190</guid>        </item>
        <item>
            <title>Review: Soluble innate immune pattern-recognition proteins for clearing dying cells and cellular components: implications on exacerbating or resolving inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=3656189&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20529971%26dopt%3DAbstract</link>
            <description>Authors: Litvack ML, Palaniyar N
    Soluble innate immune pattern-recognition proteins (sPRPs) identify non-self or altered-self molecular patterns. Dying cells often display altered-self arrays of molecules on their surfaces. Hence, sPRPs are ideal for recognizing these cells and their components. Dying cell surfaces often contain, or allow the access to different lipids, intracellular glycoproteins and nucleic acids such as DNA at different stages of cell death. These are considered as 'eat me' signals that replace the native 'don't eat me' signals such as CD31, CD47 present on the live cells. A programmed cell death process such as apoptosis also generates cell surface blebs that contain intracellular components. These blebs are easily released for effective clearance or signalling. Du...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3656189</comments>
            <pubDate>Sun, 13 Jun 2010 05:09:02 +0100</pubDate>
            <guid isPermaLink="false">3656189</guid>        </item>
        <item>
            <title>Factors determining the spontaneous activation of splenic dendritic cells in culture.</title>
            <link>http://www.medworm.com/index.php?rid=3610709&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20501515%26dopt%3DAbstract</link>
            <description>Authors: Vremec D, O'Keeffe M, Wilson A, Ferrero I, Koch U, Radtke F, Scott B, Hertzog P, Villadangos J, Shortman K
    Dendritic cells (DCs) serve as a link between the innate and adaptive immune systems. The activation state of DCs is crucial in this role. However, when DCs are isolated from lymphoid tissues, purified and placed in culture they undergo 'spontaneous' activation. The basis of this was explored, using up-regulation of DC surface MHC II, CD40, CD80 and CD86 as indicators of DC activation. No evidence was found for DC damage during isolation or for microbial products causing the activation. The culture activation of spleen DCs differed from that of Langerhans cells when released from E-cadherin-mediated adhesions, since E-cadherin was not detected and activation still occurre...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3610709</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3610709</guid>        </item>
        <item>
            <title>Contribution of the C-terminal end of apolipoprotein AI to neutralization of lipopolysaccharide endotoxic effect.</title>
            <link>http://www.medworm.com/index.php?rid=3610708&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20501516%26dopt%3DAbstract</link>
            <description>Authors: Henning MF, Herlax V, BakÃƒÂ¡s L
    It is well known that high density lipoprotein (HDL) binds bacterial lipopolysaccharide (LPS) and neutralizes its toxicity. The aim of this work was to study changes in the apolipoprotein (apo) AI structure after its interaction with LPS as well as to determine the protein domain involved in that interaction. The presented data indicate that LPS does not lead to major changes in the structure of apoAI, judging from Trp fluorescence spectra. However, analysis of denaturation behavior and binding of ANS show that LPS induces a loosened protein conformation. Further evidence for an apoAI-LPS specific interaction was obtained by incubation of the protein with (125)I-ASD-LPS. The results show that multiple regions of the protein were able to interac...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3610708</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3610708</guid>        </item>
        <item>
            <title>Cortisol is a potent modulator of lipopolysaccharide-induced interferon signaling in macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=3610707&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20501517%26dopt%3DAbstract</link>
            <description>Authors: Billing AM, Fack F, Turner JD, Muller CP
    The effects of cortisol (CORT) on resting and lipopolysaccharide (LPS)-activated monocyte-derived THP-1 macrophages were investigated by proteomics. Forty-seven proteins were found to be modulated, 20 by CORT, 11 by LPS, and 16 by CORT and LPS. Cortisol-sensitive chaperones and cytoskeletal proteins were mostly repressed. HCLS1, MGN, and MX1 were new proteins identified to be under the transcriptional control of this steroid and new CORT-sensitive variants of MX1, SYWC and IFIT3 were found. FKBP51, a known CORT target gene, showed the strongest response to CORT and synergism with LPS. In resting THP-1 macrophages, 18 proteins were modulated by CORT, with 15 being down-regulated. Activation of macrophages by LPS was associated with enhan...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3610707</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3610707</guid>        </item>
        <item>
            <title>Structural and genetic characterization of the closely related O-antigens of Escherichia coli O85 and Salmonella enterica O17.</title>
            <link>http://www.medworm.com/index.php?rid=3610706&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20501518%26dopt%3DAbstract</link>
            <description>In this study, we report on a previously undefined pair of Escherichia coli and Salmonella enterica with closely related O-antigens. The O-polysaccharides were isolated from the lipopolysaccharides of E. coli O85 and S. enterica O17 by mild acid degradation and studied by sugar analysis and NMR spectroscopy. The following structure was established for the O-unit of the E. coli O85-polysaccharide:alpha-d-Galf1 downward arrow4--&amp;gt;2)-alpha-d-Galp-(1--&amp;gt;3)-beta-d-ManpNAc-(1--&amp;gt;6)-beta-d-Galf-(1--&amp;gt;3)-beta-d-GlcpNAc-(1--&amp;gt;The S. enterica O17-polysaccharide has the same carbohydrate backbone and, in addition, contains an O-acetyl group at position 2 of approximately 80% beta-Galf residues. The O-antigen gene cluster of E. coli O85 was found to be closely related to that of S. enterica ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3610706</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3610706</guid>        </item>
        <item>
            <title>Paracellular permeability is increased by basal lipopolysaccharide in a primary culture of colonic epithelial cells; an effect prevented by an activator of Toll-like receptor-2.</title>
            <link>http://www.medworm.com/index.php?rid=3570452&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20472611%26dopt%3DAbstract</link>
            <description>In conclusion, LPS applied to the base of the colonic epithelial cells increased paracellular permeability by a mechanism involving caspase activation, suggesting a process by which perturbation of the gut barrier could be exacerbated. Moreover, activation of TLR2 ameliorated such effects.
    PMID: 20472611 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3570452</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3570452</guid>        </item>
        <item>
            <title>Hemin and a metabolic derivative coprohemin modulate the TLR4 pathway differently through different molecular targets.</title>
            <link>http://www.medworm.com/index.php?rid=3570451&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20472612%26dopt%3DAbstract</link>
            <description>Authors: Piazza M, Damore G, Costa B, Gioannini TL, Weiss JP, Peri F
    Heme is a prosthetic group in a large number of essential proteins that have a pivotal role in oxygen transport, storage and electron shuttling. High amounts of free heme are associated with pathological states. Recently, it has been suggested that activation of Toll-like receptor 4 (TLR4) is one of the ways in which the 'danger signal' of free heme is detected. Here, we examine the biochemical basis of the modulation of the TLR4 pathway by hemin (iron(III)-protoporphyrin IX) and its metabolic, oxidated derivative coprohemin (iron(III)-coproporphyrin I). High concentrations of hemin (50 microm) triggered TLR4-mediated IL-8 production in the human HEK293/TLR4 cell line in the absence of the co-receptors CD14 and MD-2; ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3570451</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3570451</guid>        </item>
        <item>
            <title>CD14 (C-260T) polymorphism is not associated with sudden infant death syndrome (SIDS) in a large South Australian cohort.</title>
            <link>http://www.medworm.com/index.php?rid=3570450&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20472613%26dopt%3DAbstract</link>
            <description>Authors: Highet AR, Gibson CS, Goldwater PN
    Similarities have been drawn between models of endotoxic shock and gross and microscopic pathology observed in sudden infant death syndrome (SIDS) cases. Polymorphisms in genes that influence the expression of endotoxin receptors could affect the outcome of toxaemia, and could, therefore, play a role in SIDS. The CD14 gene promoter contains a single nucleotide polymorphism that affects the level of CD14 gene expression. The TT genotype of the CD14 (C-260T) polymorphism causes a significantly higher density of CD14 receptor expression on monocytes which makes the individual more sensitive to endotoxin than those with the wild-type (CC). This investigation was designed to determine whether SIDS infants have a higher frequency of the CD14 (C-260...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3570450</comments>
            <pubDate>Thu, 13 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3570450</guid>        </item>
        <item>
            <title>Corrigendum.</title>
            <link>http://www.medworm.com/index.php?rid=3522988&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20427613%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 20427613 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3522988</comments>
            <pubDate>Tue, 27 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3522988</guid>        </item>
        <item>
            <title>Chemical and structural modifications of pulmonary collectins and their functional consequences.</title>
            <link>http://www.medworm.com/index.php?rid=3515990&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20423921%26dopt%3DAbstract</link>
            <description>Authors: Atochina-Vasserman EN, Beers MF, Gow AJ
    The lung is continuously exposed to inhaled pathogens (toxic pollutants, micro-organisms, environmental antigens, allergens) from the external environment. In the broncho-alveolar space, the critical balance between a measured protective response against harmful pathogens and an inappropriate inflammatory response to harmless particles is discerned by the innate pulmonary immune system. Among its many components, the surfactant proteins and specifically the pulmonary collectins (surfactant proteins A [SP-A] and D [SP-D]) appear to provide important contributions to the modulation of host defense and inflammation in the lung. Many studies have shown that multimerization of SP-A and SP-D are important for efficient local host defense inclu...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3515990</comments>
            <pubDate>Mon, 26 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3515990</guid>        </item>
        <item>
            <title>Chylomicrons combined with endotoxin moderate microvascular permeability.</title>
            <link>http://www.medworm.com/index.php?rid=3515989&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20423922%26dopt%3DAbstract</link>
            <description>Authors: Spitzer AL, Chuang KI, Victorino GP, Kasravi B, Curran B, Lee D, Harris HW
    Triglyceride-rich lipoprotein-bound endotoxin (CM-LPS) inhibits the host innate immune response to sepsis by attenuating the hepatocellular response to pro-inflammatory cytokine stimulation. This 'cytokine tolerance' in hepatocytes is a transient, receptor-dependent process that correlates with internalization of CM-LPS via low density lipoprotein (LDL) receptors. Since endothelial cells are integral to the immune response and similarly express LDL receptors, we hypothesized that CM-LPS could be internalized and ultimately attenuate the deleterious effects of pro-inflammatory molecules like tumor necrosis factor-alpha (TNF-alpha) and platelet activating factor (PAF) on endothelial permeability. Here, we...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3515989</comments>
            <pubDate>Mon, 26 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3515989</guid>        </item>
        <item>
            <title>Structural determinants of pattern recognition by lung collectins.</title>
            <link>http://www.medworm.com/index.php?rid=3515988&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20423923%26dopt%3DAbstract</link>
            <description>Authors: Seaton BA, Crouch EC, McCormack FX, Head JF, Hartshorn KL, Mendelsohn R
    Host defense roles for the lung collectins, surfactant protein A (SP-A) and surfactant protein D (SP-D), were first suspected in the 1980s when molecular characterization revealed their sequence homology to the acute phase reactant of serum, mannose-binding lectin. Surfactant protein A and SP-D have since been shown to play diverse and important roles in innate immunity and pulmonary homeostasis. Their location in surfactant ideally positions them to interact with air-space pathogens. Despite extensive structural similarity, the two proteins show many functional differences and considerable divergence in their interactions with microbial surface components, surfactant lipids, and other ligands. Recent crys...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3515988</comments>
            <pubDate>Mon, 26 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3515988</guid>        </item>
        <item>
            <title>Toll-like receptors and NOD-like receptors in pulmonary antibacterial immunity.</title>
            <link>http://www.medworm.com/index.php?rid=3508676&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418253%26dopt%3DAbstract</link>
            <description>Authors: Balamayooran T, Balamayooran G, Jeyaseelan S
    Lung diseases caused by bacteria are a leading cause of death in both immunocompromised and immunocompetent individuals as well as in children. Although neutrophil recruitment is critical to augment the host defence, excessive neutrophil accumulation results in life-threatening diseases, such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Therefore, it is important to modulate excessive neutrophil influx in ALI/ARDS to mitigate lung damage and mortality. A better understanding of the basic mechanisms underlying neutrophil influx is crucial to designing novel and innovative treatment strategies for ALI/ARDS. Recognition of bacteria in the lung is the critical first step leading to neutrophil influx. Patter...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508676</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508676</guid>        </item>
        <item>
            <title>Gp-340/DMBT1 in mucosal innate immunity.</title>
            <link>http://www.medworm.com/index.php?rid=3508675&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418254%26dopt%3DAbstract</link>
            <description>Authors: Madsen J, Mollenhauer J, Holmskov U
    Deleted in Malignant Brain Tumour 1 (DMBT1) is a gene that encodes alternatively spliced proteins involved in mucosal innate immunity. It also encodes a glycoprotein with a molecular mass of 340 kDa, and is referred to as gp-340 (DMBT1(gp340)) and salivary agglutinin (DMBT1(SAG)). DMBT1(gp340) is secreted into broncho-alveolar surface lining fluid whereas DMBT(SAG) is present in the saliva. The two molecules were shown to be identical and both interact with and agglutinate several Gram-negative and Gram-positive bacteria including Streptococcus mutans, a bacterium responsible for caries in the oral cavity. DMBT1(gp340) interacts with surfactant proteins A and D (SP-D). DMBT1(gp340) and SP-D can individually and together interact and agglutin...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508675</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508675</guid>        </item>
        <item>
            <title>Regulatory role of natural killer (NK) cells on antibody responses to Brucella Abortus.</title>
            <link>http://www.medworm.com/index.php?rid=3508674&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418255%26dopt%3DAbstract</link>
            <description>We report here that NK-cell depletion profoundly reduced the production of these polyclonal antibodies suggesting that activation of B cells by HKBA requires help from NK cells. This help may not be solely derived from NK-cell amplification of the cytokine circuit initiated by HKBA but may involve direct NK-B-cell interactions as suggested by results of in vitro analyses of NK induction of gamma2a mRNA by B cells. These findings have therapeutic implications in that the induction of polyclonal Ig production may be more important for altering the chronic phase rather than the acute stage of infection by B. abortus.
    PMID: 20418255 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508674</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508674</guid>        </item>
        <item>
            <title>Lipopolysaccharide induces raft domain expansion in membrane composed of a phospholipid-cholesterol-sphingomyelin ternary system.</title>
            <link>http://www.medworm.com/index.php?rid=3508673&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418256%26dopt%3DAbstract</link>
            <description>Authors: Nomura K, Maeda M, Sugase K, Kusumoto S
    The molecular behavior and interaction of Re-type lipopolysaccharide (ReLPS) and phospholipids were investigated in two different types of model membrane systems, a pure phospholipid membrane consisting of 1,2-dielaidoyl-sn-glycero-3-phosphoethanolamine (DEPE) and a raft-forming membrane composed of equimolar DEPE, sphingomyelin (SM), and cholesterol (Chol) by solid-state NMR spectroscopy. A remarkable influence of ReLPS on the property of lipid bilayer was found by analyzing the (13)C-NMR spectra. Namely, while both liquid-ordered (Lo) and liquid-disordered (Ld) phases co-exist in DEPE/SM/Chol, only the Lo phase is present in DEPE/SM/Chol/ReLPS. This clearly indicates that ReLPS induces expansion of the raft area in the raft-forming mem...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508673</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508673</guid>        </item>
        <item>
            <title>Mammalian peptidoglycan recognition proteins (PGRPs) in innate immunity.</title>
            <link>http://www.medworm.com/index.php?rid=3508672&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418257%26dopt%3DAbstract</link>
            <description>Authors: Dziarski R, Gupta D
    Peptidoglycan recognition proteins (PGRPs or PGLYRPs) are innate immunity proteins that are conserved from insects to mammals, recognize bacterial peptidoglycan, and function in antibacterial immunity and inflammation. Mammals have four PGRPs - PGLYRP1, PGLYRP2, PGLYRP3, and PGLYRP4. They are secreted proteins expressed in polymorphonuclear leukocytes (PGLYRP1), liver (PGLYRP2), or on body surfaces, mucous membranes, and in secretions (saliva, sweat) (PGLYRP3 and PGLYRP4). All PGRPs recognize bacterial peptidoglycan. Three PGRPs, PGLYRP1, PGLYRP3, and PGLYRP4 are directly bactericidal for both Gram-positive and Gram-negative bacteria and have no enzymatic activity, whereas PGLYRP2 is an N-acetylmuramoyl-l-alanine amidase that hydrolyzes bacterial cell wall ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508672</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508672</guid>        </item>
        <item>
            <title>Collectins link innate and adaptive immunity in allergic airway disease.</title>
            <link>http://www.medworm.com/index.php?rid=3508671&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418258%26dopt%3DAbstract</link>
            <description>Authors: Ledford JG, Pastva AM, Wright JR
    Although the lipoprotein complex of pulmonary surfactant has long been recognized as essential for reducing lung surface tension, its role in lung immune host defense has only relatively recently been elucidated. Surfactant-associated proteins A (SP-A) and D (SP-D) can attenuate bacterial and viral infection and inflammation by acting as opsonins and by regulating innate immune cell functions. Surfactant-associated protein A and D also interact with antigen-presenting cells and T cells, thereby linking the innate and adaptive immune systems. A recent study from our laboratory demonstrated that mice deficient in SP-A have enhanced susceptibility to airway hyper-responsiveness and lung inflammation induced by Mycoplasma pneumonia, an atypical bac...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508671</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508671</guid>        </item>
        <item>
            <title>Corrigendum.</title>
            <link>http://www.medworm.com/index.php?rid=3508670&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418259%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 20418259 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508670</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508670</guid>        </item>
        <item>
            <title>Genetic characterisation and structural analysis of the O-specific polysaccharide of Yersinia pseudotuberculosis serotype O:1c.</title>
            <link>http://www.medworm.com/index.php?rid=3508668&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418261%26dopt%3DAbstract</link>
            <description>Authors: De Castro C, Kenyon JJ, Cunneen M, Reeves PR, Molinaro A, Holst O, Skurnik M
    Many, but not all, of the current 21 serotypes of Yersinia pseudotuberculosis have been investigated with regard to the chemical structures of their O-specific polysaccharide (OPS) and the genetic basis of their biosynthesis. Completion of the genetics and structures of the remaining serotypes will enhance our understanding of the emerging relationship between genetics and structures within this species. Here, we present a structural and genetic analysis of the Y. pseudotuberculosis serotype O:1c OPS. Our results showed that this OPS has the same backbone as Y. pseudotuberculosis O:2b, but with a 3,6-dideoxy-d-ribo-hexofuranose (paratofuranose, Parf) side-branch instead of a 3,6-dideoxy-d-xylo-hexopyr...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508668</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508668</guid>        </item>
        <item>
            <title>Three-dimensional spheroid cultures of A549 and HepG2 cells exhibit different lipopolysaccharide (LPS) receptor expression and LPS-induced cytokine response compared with monolayer cultures.</title>
            <link>http://www.medworm.com/index.php?rid=3508667&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418262%26dopt%3DAbstract</link>
            <description>Authors: Liu J, Abate W, Xu J, Corry D, Kaul B, Jackson SK
    Lipopolysaccharide (LPS) is a potent modulator of pathogen-induced host inflammatory responses. Lipopolysaccharide signaling to host cells is correlated with the expression of well-characterized LPS receptors. We have developed three-dimensional (3-D) cell cultures (spheroids) that are more representative of in vivo conditions than traditional monolayer cultures and may provide novel in vitro models to study the inflammatory response. In this work, we have compared F-actin organization, LPS-induced pro-inflammatory cytokine response and LPS receptor expression between spheroid and monolayer cultures from A549 lung epithelial cells and HepG2 hepatocytes. Significant junctional F-actin was seen at the cell-cell contact points thr...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508667</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508667</guid>        </item>
        <item>
            <title>Defensins and cathelicidins in lung immunity.</title>
            <link>http://www.medworm.com/index.php?rid=3508666&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20418263%26dopt%3DAbstract</link>
            <description>Authors: Tecle T, Tripathi S, Hartshorn KL
    Defensins were first identified in 1985 and are now recognized as part of a large family of antimicrobial peptides, divided into three categories: alpha-, beta-, and -defensins. These defensin classes differ in structure, sites of expression and biological activities. Human alpha-defensins include peptides that are expressed primarily in neutrophils, whereas human beta-defensins are widely expressed in epithelial cells, including those lining the respiratory tract. Defensins were first studied for their broad spectrum activity against bacteria, fungi and viruses; however, it is now clear that they also recruit inflammatory cells and promote innate and adaptive immune responses. Recent evidence shows that defensins have anti-inflammatory effect...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3508666</comments>
            <pubDate>Thu, 22 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3508666</guid>        </item>
        <item>
            <title>NAD+: a modulator of immune functions.</title>
            <link>http://www.medworm.com/index.php?rid=3476316&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20388721%26dopt%3DAbstract</link>
            <description>Authors: Grahnert A, Grahnert A, Klein C, Schilling E, Wehrhahn J, Hauschildt S
    Latterly, nicotinamide adenine dinucleotide (NAD(+)) has emerged as a molecule with versatile functions and of enormous impact on the maintenance of cell integrity. Besides playing key roles in almost all major aspects of energy metabolism, there is mounting evidence that NAD(+) and its degradation products affect various biological activities including calcium homeostasis, gene transcription, DNA repair, and intercellular communication. This review is aimed at giving a brief insight into the life cycle of NAD(+) in the cell, referring to synthesis, action and degradation aspects. With respect to their immunological relevance, the importance and function of the major NAD(+) metabolizing enzymes, namely CD38...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3476316</comments>
            <pubDate>Mon, 12 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3476316</guid>        </item>
        <item>
            <title>Referees 2009.</title>
            <link>http://www.medworm.com/index.php?rid=3412847&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20338907%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 20338907 [PubMed - in process] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3412847</comments>
            <pubDate>Mon, 29 Mar 2010 05:16:02 +0100</pubDate>
            <guid isPermaLink="false">3412847</guid>        </item>
        <item>
            <title>Structure and serology of O-antigens as the basis for classification of Proteus strains.</title>
            <link>http://www.medworm.com/index.php?rid=3392157&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20305038%26dopt%3DAbstract</link>
            <description>Authors: Knirel YA, Perepelov AV, Kondakova AN, Senchenkova SN, Sidorczyk Z, Rozalski A, Kaca W
    This review is devoted to structural and serological characteristics of the O-antigens (O-polysaccharides) of the lipopolysaccharides of various Proteus species, which provide the basis for classifying Proteus strains to O-serogroups. The antigenic relationships of Proteus strains within and beyond the genus as well as their O-antigen-related bioactivities are also discussed.
    PMID: 20305038 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3392157</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3392157</guid>        </item>
        <item>
            <title>Pretreatment with lipopolysaccharide modulates innate immunity in corneal fibroblasts challenged with Aspergillus fumigatus.</title>
            <link>http://www.medworm.com/index.php?rid=3392156&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20305039%26dopt%3DAbstract</link>
            <description>In this study, we tested the hypothesis that lipopolysaccharide (LPS), a ligand of TLR4, can induce tolerance of A. fumigatus hyphae in telomerase-immortalized human stroma fibroblasts (THSFs). The THSFs were pretreated with low-dose LPS for various times and then challenged with A. fumigatus hyphae. We observed that pretreatment of THSFs with low-dose LPS resulted in diminished production of cytokines IL-8 and IL-6 and elevated expression of antimicrobial peptides, such as CC chemokine-ligand 20 (CCL20) and thymosin beta4 (Tbeta4), upon subsequent A. fumigatus challenge. Furthermore, LPS pretreatment also resulted in suppression of polymorphonuclear leukocyte (PMN) migration. Our results suggested that THSFs pretreated with LPS develop a state of A. fumigatus hyphae tolerance. This may in...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3392156</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3392156</guid>        </item>
        <item>
            <title>Surfactant protein-A enhances ureaplasmacidal activity in Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3331725&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20197455%26dopt%3DAbstract</link>
            <description>Conclusions: These in vitro data confirm that SP-A is important in host defense to perinatally-acquired Ureaplasma infection.
    PMID: 20197455 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331725</comments>
            <pubDate>Tue, 02 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3331725</guid>        </item>
        <item>
            <title>Interferon-gamma secretion is induced in IL-12 stimulated human NK cells by recognition of Helicobacter pylori or TLR2 ligands.</title>
            <link>http://www.medworm.com/index.php?rid=3246041&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20130107%26dopt%3DAbstract</link>
            <description>In conclusion, we suggest an involvement of TLR2 in the recognition of H. pylori by human NK cells and that HpaA is a TLR2 ligand important for recognition.
    PMID: 20130107 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3246041</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3246041</guid>        </item>
        <item>
            <title>1H and hyperpolarized 3He magnetic resonance imaging clearly detect the preventative effect of a glucocorticoid on endotoxin-induced pulmonary inflammation in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3246040&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20130108%26dopt%3DAbstract</link>
            <description>Conclusions: Hyperpolarized (3)He MRI and (1)H MRI clearly visualized the preventative effect of budesonide on the impact of endotoxin on pulmonary ventilation and edema, respectively. The fact that ventilation defects on (3)He MRI corresponded to findings from conventional (1)H MRI, as well as to counts of BAL inflammatory cells suggests that these imaging techniques constitute promising tools for non-invasive monitoring of pulmonary inflammation in vivo.
    PMID: 20130108 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3246040</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3246040</guid>        </item>
        <item>
            <title>Identification of putative innate immune related genes from a cell line of the mosquito Aedes albopictus following bacterial challenge.</title>
            <link>http://www.medworm.com/index.php?rid=3239939&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20123933%26dopt%3DAbstract</link>
            <description>We report identification of putative innate immune related genes from a cell line of the mosquito Aedes albopictus challenged with heat-killed bacteria. Using a subtractive hybridization and sequencing approach, we analyzed a total 309 expressed sequence tags (ESTs) which clustered in 40 contigs. Thirty-five percent of genes yielded homology to known immune genes corresponding to antimicrobial peptides (AMPs), pathogen-associated molecular patterns, protease and immune signaling cascades. Interestingly, most of the genes have not been previously described from this mosquito and thus represent a class of novel immune genes. Further, 25% sequences did not match to any known species in the non-redundant databases, appear to be specific to the mosquito A. albopictus and merit further study.
  ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3239939</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3239939</guid>        </item>
        <item>
            <title>Endotoxin, zymosan, and cytokines decrease the expression of the transcription factor, carbohydrate response element binding protein, and its target genes.</title>
            <link>http://www.medworm.com/index.php?rid=3213303&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20100709%26dopt%3DAbstract</link>
            <description>Authors: Feingold KR, Shigenaga JK, Patzek SM, Chui LG, Moser A, Grunfeld C
    Carbohydrate response element binding protein (ChREBP) is a recently discovered transcription factor whose levels and activity are increased by glucose leading to the activation of target genes, which include acetyl-CoA carboxylase, fatty acid synthase, and liver-type pyruvate kinase. Here, we demonstrate that lipopolysaccharide (LPS) treatment causes a marked decrease in ChREBP mRNA and protein levels in the liver of mice fed a normal chow diet or in mice fasted for 24 h and then re-fed a high carbohydrate diet. This decrease occurs rapidly and is a sensitive response (half-maximal dose 0.1 mug/mouse). The decrease in ChREBP is accompanied by a decrease in the expression of ChREBP target genes. Zymosan and tur...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213303</comments>
            <pubDate>Mon, 25 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213303</guid>        </item>
        <item>
            <title>Identifying the functional part of heparin-binding protein (HBP) as a monocyte stimulator and the novel role of monocytes as HBP producers.</title>
            <link>http://www.medworm.com/index.php?rid=3189617&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083497%26dopt%3DAbstract</link>
            <description>Authors: Schou M, Djurup R, Norris K, Flodgaard H
    Heparin-binding protein (HBP), an evolutionary ancient and biologically highly important molecule in inflammation, is an inactive serine protease due to mutations in the catalytic triad. The histidine (position 41) in the conserved sequence TAAHC is mutated to serine and this sequence (TAASC) plays a crucial role when HBP binds to monocytes. We synthesized a 20-44 HBP peptide, cyclicized by a sulphur bridge, which encompasses this amino acid and functions as full-length HBP. Using a human monocyte cell line, we have shown that lipopolysaccharide (LPS)-triggered secretion of IL-6 is enhanced up to 10-fold when full-length HBP or the peptide are present in low-to-moderate concentrations. A monoclonal antibody neutralizing HBP also neutral...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189617</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189617</guid>        </item>
        <item>
            <title>Telling apart friend from foe: Discriminating between commensals and pathogens at mucosal sites.</title>
            <link>http://www.medworm.com/index.php?rid=3189616&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083498%26dopt%3DAbstract</link>
            <description>Authors: Srinivasan N
    From the moment we are born, we are exposed to a vast variety of microbes. The intestine in particular is perhaps inhabited by the largest number of microbes, consisting of both established commensals as well as sporadic pathogens. Mucosal surfaces form an important barrier against microbial invasion. Together with the physical barrier that they provide, mucosal surfaces also rely on innate immune functions to sense luminal microbes and signal accordingly to generate protective immune responses. However, since innate immune recognition is microbial specific and antigen-independent, the contact with both beneficial commensals and harmful pathogens creates the need for discrimination between the two. The mechanisms governing the ability of the mucosal immune system ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189616</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189616</guid>        </item>
        <item>
            <title>Endotoxin recognition in fish results in inflammatory cytokine secretion not gene expression.</title>
            <link>http://www.medworm.com/index.php?rid=3189615&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083499%26dopt%3DAbstract</link>
            <description>Authors: Roher N, Callol A, Planas JV, Goetz FW, Mackenzie SA
    Macrophages are phagocytes that have a central role in the organization of the immune system after an infection. These cells can recognize specific molecular components of micro-organisms (pathogen-associated molecular patterns, PAMPs) via specific receptors (PRRs) and elicit specific cellular responses. In the past, the expression of immune genes in response to different PAMPs has been characterized in different fish species. However, little is known about actual cytokine release. We characterized the secretion of tumour necrosis factor (TNF)-alpha in primary macrophage cultures of rainbow trout (Oncorhynchus mykiss) in response to several PAMPs by Western blot and compared this to the induction of TNF-alpha gene expression...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189615</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189615</guid>        </item>
        <item>
            <title>Analgesic effects of chemically synthesized NO1 and NOD2 agonists in mice.</title>
            <link>http://www.medworm.com/index.php?rid=3189614&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083500%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated the analgesic activities of NOD1 as well as NOD2 agonists. Intravenous injection of NOD2-agonistic MDP, 6-O-stearoyl-MDP (L18-MDP), and MDP-Lys (L18) exhibited analgesic activity at 10, 50, and 2.0 mug/head, respectively, in BALB/c mice. NOD1-Agonistic FK156 (d-lactyl-l-Ala-d-Glu-meso-DAP-l-Gly) and FK565 (heptanoyl-d-Glu-meso-DAP-d-Ala) were also analgesic at 50 mug/head and 1.0 mug/head, respectively. The analgesic effect of FK565 appeared from 30 min, reached maximum activity at 8 h, and continued until 24 h. The FK565 exhibited activity by various administration routes; intravenous, intraperitoneal, intramuscular, sublingual (1.0 mug/head each), subcutaneous, intragastric (oral), intragingival (10 mug/head each) and intracerebroventricular (0.01 mug/head)...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189614</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189614</guid>        </item>
        <item>
            <title>CpG oligodeoxynucleotide and double-stranded RNA synergize to enhance nitric oxide production and mRNA expression of inducible nitric oxide synthase, pro-inflammatory cytokines, and chemokines in chicken monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3189613&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083501%26dopt%3DAbstract</link>
            <description>Authors: He H, Mackinnon KM, Genovese KJ, Kogut MH
    Toll-like receptors (TLRs) recognize microbial components and initiate the innate immune responses that control microbial infections. The interaction between ligands of TLR3 and TLR9, poly I:C (an analog of viral double-stranded RNA) and CpG-ODN (a CpG-motif containing oligodeoxydinucleotide) on the inflammatory immune responses, including the production of nitric oxide (NO) and the expression of inducible NO synthase (iNOS), pro-inflammatory cytokines interleukin (IL)-1beta and IL-6, and chemokines IL-8 and macrophage inflammatory protein (MIP)-1beta, were investigated in chicken monocytes. The NO production was significantly higher when stimulated with a combination of CpG-ODN and poly I:C than with either CpG-ODN or poly I:C alone. ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189613</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189613</guid>        </item>
        <item>
            <title>Antiserum against Raoultella terrigena ATCC 33257 identifies a large number of Raoultella and Klebsiella clinical isolates as serotype 012.</title>
            <link>http://www.medworm.com/index.php?rid=3156702&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20053705%26dopt%3DAbstract</link>
            <description>Authors: Mertens K, M&amp;#xFC;ller-Loennies S, Stengel P, Podschun R, Hansen DS, Mamat U
    Raoultella terrigena ATCC 33257, recently reclassified from the genus Klebsiella, is a drinking water isolate and belongs to a large group of non-typeable Klebsiella and Raoultella strains. Using an O-antiserum against a capsule-deficient mutant of this strain, we could show a high prevalence (10.5%) of the R. terrigena O-serotype among non-typeable, clinical Klebsiella and Raoultella isolates. We observed a strong serological cross-reaction with the K. pneumoniae O12 reference strain, indicating that a large percentage of these non-typeable strains may belong to the O12 serotype, although these are currently not detectable by the K. pneumoniae O12 reference antiserum in use. Therefore, we analyzed th...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3156702</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3156702</guid>        </item>
        <item>
            <title>ONO 3403, a synthetic serine protease inhibitor, inhibits lipopolysaccharide-induced tumor necrosis factor-{alpha} and nitric oxide production and protects mice from lethal endotoxic shock.</title>
            <link>http://www.medworm.com/index.php?rid=3115668&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20023007%26dopt%3DAbstract</link>
            <description>Authors: Tumurkhuu G, Koide N, Hiwasa T, Ookoshi M, Dagvadorj J, Noman AS, Iftakhar-E-Khuda I, Naiki Y, Komatsu T, Yoshida T, Yokochi T
    ONO 3403, a new synthetic serine protease inhibitor, is a derivative of camostat mesilate and has a higher protease-inhibitory activity. The effect of ONO 3403 on lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-alpha and nitric oxide (NO) production in RAW 264.7 macrophage-like cells was examined. ONO 3403 significantly inhibited LPS-induced TNF-alpha production at a lower concentration than camostat mesilate. It also inhibited LPS-induced NO production. Their inhibition was responsible for the reduced mRNA expression of TNF-alpha and inducible NO synthase. In LPS-stimulated cells, ONO 3403 prevented the augmentation of MyD88 expression an...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3115668</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3115668</guid>        </item>
        <item>
            <title>Differential responses of epithelial Sertoli cells of the rat testis to Toll-Like receptor 2 and 4 ligands: implications for studies of testicular inflammation using bacterial lipopolysaccharides.</title>
            <link>http://www.medworm.com/index.php?rid=3115667&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20023008%26dopt%3DAbstract</link>
            <description>Authors: Winnall WR, Muir JA, Hedger MP
    The relative contribution of epithelial Sertoli cells in response to bacterial infection of the testis remains poorly characterised, since studies on inflammatory properties of these cells have invariably used unpurified lipopolysaccharide (LPS) preparations contaminated with bacterial lipopeptides. Consequently, isolated rat Sertoli cells were stimulated with either unextracted or phenol re-extracted LPS, and analysed for Toll-like receptor (TLR) 4, TLR2 and inflammatory cytokine gene expression by quantitative reverse transcription polymerase chain reaction (RT-PCR). Expression of TLR4 and its co-receptor protein myeloid differentiation (MD) 2 in Sertoli cells and testicular macrophages were similar, but Sertoli cells displayed low basal or LPS...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3115667</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3115667</guid>        </item>
        <item>
            <title>Low mannose-binding lectin levels and MBL2 gene polymorphisms associate with Chlamydia pneumoniae antibodies.</title>
            <link>http://www.medworm.com/index.php?rid=3076142&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19969625%26dopt%3DAbstract</link>
            <description>Conclusions: These results suggest, for the first time, that low serum MBL levels and MBL2 polymorphisms may associate with elevated C. pneumoniae antibodies and seroconversions and thus support the previous findings in vitro.
    PMID: 19969625 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3076142</comments>
            <pubDate>Mon, 07 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3076142</guid>        </item>
        <item>
            <title>Sesamol downregulates the lipopolysaccharide-induced inflammatory response by inhibiting nuclear factor-kappa B activation.</title>
            <link>http://www.medworm.com/index.php?rid=3034356&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19939906%26dopt%3DAbstract</link>
            <description>We examined the effects of sesamol on the lipopolysaccharide (LPS)-induced inflammatory response. Sesamol inhibited serum tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and nitrite production in LPS-treated mice, and inhibited LPS-induced inducible nitric oxide synthase expression in mouse leukocytes. Sesamol also down-regulated TNF-alpha, IL-1beta, and nitrite production as well as inducible nitric oxide synthase expression in LPS-treated RAW 264.7 cells. Further, sesamol inhibited LPS-induced nuclear factor (NF)-kappaB translocation and inhibitor (I)kappaB-alpha phosphorylation in RAW 264.7 cells. By inhibiting TNF-alpha, IL-1beta, and nitrite levels, and interfering with the NF-kappaB pathway, sesamol down-regulated the LPS-initiated inflammatory response.
    PMID: 19939906 ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3034356</comments>
            <pubDate>Wed, 25 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3034356</guid>        </item>
        <item>
            <title>Interleukin-6 is essential for zwitterionic polysaccharide-mediated abscess formation.</title>
            <link>http://www.medworm.com/index.php?rid=2978300&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19897529%26dopt%3DAbstract</link>
            <description>Authors: Meemboor S, Mertens J, Flenner E, Groneck L, Zingarelli A, Gamst&amp;#xE4;tter T, Bessler M, Seeger JM, Kashkar H, Odenthal M, Kalka-Moll WM
    Abscess formation associated with secondary peritonitis causes severe morbidity and can be fatal. Formation of abscesses requires the presence of CD4(+) T-cells. Zwitterionic polysaccharides (ZPSs) represent a novel class of immunomodulatory bacterial antigens that stimulate CD4(+) T-cells in a major histocompatibility complex (MHC) class II-dependent manner. The capsular polysaccharide Sp1 of Streptococcus pneumoniae serotype 1 possesses a zwitterionic charge with free amino groups and promotes T-cell-dependent abscess formation in an experimental mouse model. So far, nothing is known about the function of Interleukin (IL)-6 in intraperitone...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2978300</comments>
            <pubDate>Fri, 06 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2978300</guid>        </item>
        <item>
            <title>Transcriptional profiling at different sites in lungs of pigs during acute bacterial respiratory infection.</title>
            <link>http://www.medworm.com/index.php?rid=2978299&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19897530%26dopt%3DAbstract</link>
            <description>In conclusion, we found subsets of genes expressed at different levels in the three selected areas of the infected lung as compared to the control group. Thus it is demonstrated that an infection with clearly defined infected loci leads to a rapid disseminated intra-organ response in neighbouring seemingly unaffected tissue areas of the infected organ. Within the lung, we found a clear division of induced genes as, in unaffected areas a large part of differently expressed genes were involved in systemic reactions to infections, while differently expressed genes in necrotic areas were mainly concerned with homeostasis regulation.
    PMID: 19897530 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2978299</comments>
            <pubDate>Fri, 06 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2978299</guid>        </item>
        <item>
            <title>Muramyldipeptide augments the actions of lipopolysaccharide in mice by stimulating macrophages to produce pro-IL-1B and by down-regulation of suppressor of cytokine signaling 1 (SOCS1).</title>
            <link>http://www.medworm.com/index.php?rid=2978298&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19897531%26dopt%3DAbstract</link>
            <description>Authors: Shikama Y, Kuroishi T, Nagai Y, Iwakura Y, Shimauchi H, Takada H, Sugawara S, Endo Y
    Muramyldipeptide (MDP), the minimum essential structure responsible for the immuno-adjuvant activity of peptidoglycan, is recognized by intracellular nuclear-binding oligomerization domain 2 (NOD2). Muramyldipeptide enhances the activities of lipopolysaccharide (LPS), but the mechanism underlying this effect is unclear. Here, we obtained evidence that intravenously injected MDP augments LPS-induced hypothermia in wild-type mice, but not in mice deficient in interleukin (IL)-1alpha/beta and/or tumor-necrosis factor (TNF)-alpha. Muramyldipeptide also: (i) increased pro-IL-1beta in tissues, but did not increase IL-1beta in serum (since caspase-1 was not activated by MDP); (ii) down-regulated the ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2978298</comments>
            <pubDate>Fri, 06 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2978298</guid>        </item>
        <item>
            <title>Expression of NOD2 is increased in inflamed human dental pulps and lipoteichoic acid-stimulated odontoblast-like cells.</title>
            <link>http://www.medworm.com/index.php?rid=2955305&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19880660%26dopt%3DAbstract</link>
            <description>In this study, we investigated NOD2 expression in healthy and inflamed human dental pulps challenged by bacteria, and in cultured odontoblast-like cells stimulated with lipoteichoic acid (LTA), a Toll-like receptor (TLR) 2 agonist which is specific for Gram-positive bacteria. We found that NOD2 gene expression was significantly up-regulated in pulps with acute inflammation compared to healthy ones. In vitro, LTA augmented NOD2 gene expression and protein level in odontoblast-like cells. The increase was more pronounced in odontoblast-like cells compared to dental pulp fibroblasts. Blocking experiments in odontoblast-like cells with anti-TLR2 antibody strongly reduced the NOD2 gene expression increase, whereas stimulation with the synthetic TLR2 ligand Pam2CSK4 confirmed NOD2 gene up-regula...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2955305</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2955305</guid>        </item>
        <item>
            <title>The lipid A of Burkholderia multivorans C1576 smooth-type lipopolysaccharide and its pro-inflammatory activity in a cystic fibrosis airways model.</title>
            <link>http://www.medworm.com/index.php?rid=2955304&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19880661%26dopt%3DAbstract</link>
            <description>Authors: Ierano T, Cescutti P, Leone MR, Luciani A, Rizzo R, Raia V, Lanzetta R, Parrilli M, Maiuri L, Silipo A, Molinaro A
    Cystic fibrosis is an autosomal recessive disorder and it is characterised by chronic bacterial airway infection which leads to progressive lung deterioration, sometimes with fatal outcome. Burkholderia multivorans and Burkholderia cenocepacia are the species responsible for most of the infections of cystic fibrosis patients. Lipopolysaccharide endotoxins (LPSs) are among the foremost factors of pathogenesis of Gram-negative infection and, in particular, lipid A is the endotoxic portion of LPS responsible for eliciting host innate immune response. In this work, the complete primary structure of the lipid A from B. multivorans C1576 has been defined and, further, i...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2955304</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2955304</guid>        </item>
        <item>
            <title>Enhanced antibody responses to a detoxified lipopolysaccharide-group B meningococcal outer membrane protein vaccine are due to synergistic engagement of Toll-like receptors.</title>
            <link>http://www.medworm.com/index.php?rid=2891071&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19822632%26dopt%3DAbstract</link>
            <description>Authors: Chen WH, Basu S, Bhattacharjee AK, Cross AS
    When given passively or elicited actively, antibodies induced by a detoxified Escherichia coli Rc chemotype (J5) mutant lipopolysaccharide (J5dLPS)-group B meningococcal outer membrane protein (OMP) complex vaccine protected animals from lethal sepsis. The protection from sepsis is believed to be dependent on high levels of antibodies against the core glycolipid (CGL), a region of LPS that is rather conserved among Enterobacteriaceae. The addition of unmethylated deoxycytidyl-deoxyguanosine dinucleotide (CpG)-containing oligodeoxynucleotides (ODN) was used as an immuno-adjuvant to improve antibody responses. In preparation for a Phase I human trial, we elucidated potential contributions by which the sepsis vaccine (J5dLPS-OMP) and Cp...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2891071</comments>
            <pubDate>Sun, 11 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2891071</guid>        </item>
        <item>
            <title>Platelet factor 4 (CXCL4) facilitates human macrophage infection with HIV-1 and potentiates virus replication.</title>
            <link>http://www.medworm.com/index.php?rid=2832683&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19773294%26dopt%3DAbstract</link>
            <description>In this study, CXCL4-derived macrophages are compared with macrophage-colony stimulating factor (M-CSF)-derived macrophages for their ability to support HIV-1 replication. We show that CXCL4-derived macrophages can be infected with macrophage-tropic HIV-1 that uses either CC-chemokine receptor 5 (CCR5) or CXC-chemokine receptor 4 (CXCR4) as a co-receptor for viral entry. We also find that M-CSF and the chemokines, monocyte chemoattractant protein 1 (MCP-1; CCL2) and macrophage-inflammatory-protein-1-alpha (MIP-1alpha; CCL3) are produced upon R5- and X4-tropic HIV-1 replication in both M-CSF- and CXCL4-derived human macrophages. In addition, CXCL4 added to M-CSF-derived macrophages after virus adsorption and maintained throughout the infection enhances HIV-1 replication. We thus propose a n...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2832683</comments>
            <pubDate>Mon, 21 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2832683</guid>        </item>
        <item>
            <title>Characterization of the O-polysaccharide structure and biosynthetic gene cluster of Yersinia pseudotuberculosis serotype O:15.</title>
            <link>http://www.medworm.com/index.php?rid=2762452&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19723831%26dopt%3DAbstract</link>
            <description>Authors: De Castro C, Skurnik M, Molinaro A, Holst O
    Yersinia pseudotuberculosis serotyping scheme contains 21 serotypes based on the distribution of about 30 different O-factors within the species. The chemical structures of LPSs and the genetic basis of their biosynthesis has been determined for a number of Y. pseudotuberculosis strains representing different serotypes; thus, an overall picture of the relationship between genetics and structures is emerging. In this work, we have performed a structural and genetic analysis of the Y. pseudotuberculosis serotype O:15 O-specific polysaccharide. Our results showed that the set-up of the Y. pseudotuberculosis O:15 gene cluster is a hybrid between those of Y. pseudotuberculosis serotypes O:1b and O:5a, possibly due to a single recombinatio...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2762452</comments>
            <pubDate>Mon, 31 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2762452</guid>        </item>
        <item>
            <title>Lactoferrin decreases LPS-induced mitochondrial dysfunction in cultured cells and in animal endotoxemia model.</title>
            <link>http://www.medworm.com/index.php?rid=2762451&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19723832%26dopt%3DAbstract</link>
            <description>Authors: Kruzel ML, Actor JK, Radak Z, Bacsi A, Saavedra-Molina A, Boldogh I
    Lactoferrin is a non-heme iron-binding glycoprotein, produced by mucosal epithelial cells and granulocytes in most mammalian species. It is involved in regulation of immune responses, possesses anti-oxidant, anti-carcinogenic, anti-inflammatory properties, and provides protection against various microbial infections. In addition, lactoferrin has been implicated in protection against the development of insult-induced systemic inflammatory response syndrome (SIRS) and its progression into septic conditions in vivo. Here we show a potential mechanism by which lactoferrin lessens oxidative insult at the cellular and tissue levels after lipopolysaccharide (LPS) exposure. Lactoferrin pretreatment of cells decreased ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2762451</comments>
            <pubDate>Mon, 31 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2762451</guid>        </item>
        <item>
            <title>Class C CpG oligodeoxynucleotides as a single agent and in combination with radiotherapy efficiently delayed growth of subcutaneous B16F1 tumors.</title>
            <link>http://www.medworm.com/index.php?rid=2762450&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19723833%26dopt%3DAbstract</link>
            <description>In conclusion, the combined therapy with CpG ODNs and irradiation creates a unique in situ DCs vaccine that could be easily applicable without prior knowledge of tumor antigens.
    PMID: 19723833 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2762450</comments>
            <pubDate>Mon, 31 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2762450</guid>        </item>
        <item>
            <title>Differential effect of molecular weight hyaluronan on lipopolysaccharide-induced damage in chondrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2742925&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710088%26dopt%3DAbstract</link>
            <description>Authors: Campo GM, Avenoso A, Campo S, D'Ascola A, Traina P, Rugolo CA, Calatroni A
    Hyaluronan is a biological polysaccharide that may exist in different degrees of polymerization. Several investigations reported that low molecular mass hyaluronan may have pro-inflammatory activity, while high molecular mass hyaluronan can exert beneficial effects. Starting from these data, the aim of this study was to investigate the effect of hyaluronan of different molecular mass in mouse articular chondrocyte cultures stimulated with lipopolysaccharide (LPS). Inflammation was induced in chondrocytes by acute treatment with 2.0 microg/ml LPS. High levels of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, interferon (IFN)-gamma and iNOS gene expression and their related proteins wer...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742925</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742925</guid>        </item>
        <item>
            <title>Endotoxin tolerance does not limit mild ischemia-reperfusion injury in humans in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=2742924&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710089%26dopt%3DAbstract</link>
            <description>Authors: Draisma A, de Goeij M, Wouters CW, Riksen NP, Oyen WJ, Rongen GA, Boerman OC, van Deuren M, van der Hoeven JG, Pickkers P
    Animal studies have shown that previous exposure to lipopolysaccharide (LPS) can limit ischemia-reperfusion injury. We tested whether pretreatment with LPS also protects against ischemia-reperfusion injury in humans in vivo. Fourteen volunteers received bolus injections of incremental dosages of LPS on 5 consecutive days (LPS group). Before the first and 1 day after the last LPS administration, the forearm circulation of the non-dominant arm was occluded for 10 min, with concomitant intermittent handgripping to induce transient ischemia. After reperfusion, 0.1 mg of (99m)Tc-labeled annexin A5 (400 MBq) was injected intravenously to detect phosphatidylserine...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742924</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742924</guid>        </item>
        <item>
            <title>A Mycobacterium avium subsp. paratuberculosis LuxR regulates cell envelope and virulence.</title>
            <link>http://www.medworm.com/index.php?rid=2742923&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710090%26dopt%3DAbstract</link>
            <description>Authors: Alonso-Hearn M, Eckstein TM, Sommer S, Bermudez LE
    Mycobacterium avium subsp. paratuberculosis adapts to the environment via the regulation of genes affecting its envelope's composition. Bacteria grown in milk (in vivo conditions) presented differences in the cell wall-associated lipids and in the expression of genes involved in lipid metabolism (FadE8, FadE6 and MAP1420) and host cell invasion (MAP1203, LprL). A different lipid profile was also observed in the envelope of intracellular bacteria after 1 h of infection. Intracellular bacteria showed up-regulation of a LuxR regulator which controls the envelope's composition by up-regulation of FadE8, MAP1420, MAP1203 and LprL and by down-regulation of pks12, mmpL2 and MAP2594. A LuxR-overexpressing strain with a lipid-deficient...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742923</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742923</guid>        </item>
        <item>
            <title>Lipopolysaccharide Stimulated Whole Blood Cytokine Production Does not Predict the Inflammatory Response in Human Endotoxemia.</title>
            <link>http://www.medworm.com/index.php?rid=2742921&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710091%26dopt%3DAbstract</link>
            <description>Authors: Dorresteijn MJ, Draisma A, van der Hoeven JG, Pickkers P
    A widely applied method to study the activation of the innate immune system is in vitro stimulation of whole blood using lipopolysaccharide (LPS). However, it is unclear if in vitro cytokine production relates to in vivo cytokine levels elicited during experimental endotoxemia or sepsis. To determine the correlation between in vitro cytokine production and the in vivo inflammatory response, blood was obtained from 15 healthy volunteers for in vitro incubation with Escherichia coli LPS, immediately followed by experimental E. coli endotoxemia. Correlations of in vitro and peak in vivo cytokine concentrations were determined using Pearson correlation coefficient. In stimulated whole blood, tumor necrosis factor (TNF)-alpha...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742921</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742921</guid>        </item>
        <item>
            <title>Monitoring of endothelial cell activation in experimental sepsis with a two-step cell culture model.</title>
            <link>http://www.medworm.com/index.php?rid=2742912&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710092%26dopt%3DAbstract</link>
            <description>Authors: Schildberger A, Rossmanith E, Weber V, Falkenhagen D
    The aim of this work was to establish and characterize a cell culture model for lipopolysaccharide (LPS)-induced activation of human endothelial cells. Monocytic THP-1 cells were stimulated for 4 h with 10 ng/ml LPS from Pseudomonas aeruginosa in media containing 10% human plasma. Culture supernatants containing LPS and factors secreted by THP-1 in response to stimulation were applied to human umbilical vein endothelial cells (HUVECs). Nuclear factor-kappaB (NF-kappaB) activity, expression of adhesion molecules, and cytokine secretion were quantified. In addition, the effect of adsorptive removal of tumour necrosis factor-alpha (TNF-alpha) from the THP-1 culture supernatant on HUVEC activation was assessed. After 4 h of stim...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742912</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742912</guid>        </item>
        <item>
            <title>PLC, p38/MAPK, and NF{kappa} B-mediated induction of MIP-3{alpha}/CCL20 by porphyromonas gingivalis.</title>
            <link>http://www.medworm.com/index.php?rid=2742905&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710093%26dopt%3DAbstract</link>
            <description>Authors: Dommisch H, Chung WO, Jepsen S, Hacker BM, Dale BA
    Macrophage inflammatory protein-3alpha/C-C chemokine ligand 20 (MIP-3alpha/CCL20) is an antimicrobial peptide that plays an important role in innate immunity. In addition to direct microbicidal effects, MIP-3alpha/CCL20 also exhibits cytokine-like functions that are critical during dendritic cell activation. The aim of the present study was to investigate further which signaling pathways are involved in the MIP-3alpha/CCL20 mRNA expression in response to whole-cell Porphyromonas gingivalis. Primary gingival epithelial cells (GECs) and the immortalized oral keratinocyte cell-line OKF6/TERT-2 were stimulated with whole-cell P. gingivalis. Prior to stimulation, GECs and OKF6/TERT-2 cells were pretreated with specific inhibitors f...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742905</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742905</guid>        </item>
        <item>
            <title>Hepatic gene expression changes in pigs experimentally infected with the lung pathogen Actinobacillus pleuropneumoniae as analysed with an innate immunity focused microarray.</title>
            <link>http://www.medworm.com/index.php?rid=2742904&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710094%26dopt%3DAbstract</link>
            <description>Authors: Skovgaard K, Mortensen S, Boye M, Hedegaard J, Heegaard PM
    Knowledge on gene expression in the liver during respiratory infections is limited although it is well-established that this organ is an important site of synthesis of several systemic innate immune components as response to infections. In the present study, the early transcriptional hepatic response of genes associated with innate immune responses was studied in pigs 14-18 h after intranasal inoculation with Actinobacillus pleuropneumoniae, using innate immune focused microarrays and quantitative real-time PCR (qPCR). The microarray analysis of liver tissue established that 51 genes were differentially expressed. A large group of these genes encoded proteins involved in the acute phase response, including serum amyloi...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742904</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742904</guid>        </item>
        <item>
            <title>The non-peptide chemical 3,4-methylenedioxyphenol blocked lipopolysaccharide (LPS) from binding to LPS-binding protein and inhibited pro-inflammatory cytokines.</title>
            <link>http://www.medworm.com/index.php?rid=2742903&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710095%26dopt%3DAbstract</link>
            <description>Authors: Hsu DZ, Chu PY, Liu MY
    After binding to lipopolysaccharide (LPS)-binding protein, LPS is transferred to CD14 and then to the MD2-Toll-like receptor 4 complex, which results in the progression of sepsis. We investigated how 3,4-methylenedioxyphenol (sesamol), an inexpensive natural product in sesame seeds, affects the binding of LPS and LPS-binding protein and the release of pro-inflammatory cytokines. Sesamol: (i) dose-dependently inhibited LPS from binding to LPS binding protein; (ii) significantly decreased the release of tumor necrosis factor-alpha and interleukin-1beta in LPS-challenged peritoneal macrophages in medium and in the serum of LPS-challenged rats; and (iii) significantly reduced the mortality rate in mice given a lethal dose of LPS. We hypothesize that sesamol ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742903</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742903</guid>        </item>
        <item>
            <title>Anti-inflammatory effects of c1-Inhibitor in porcine and human whole blood are independent of its protease inhibition activity.</title>
            <link>http://www.medworm.com/index.php?rid=2742902&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710096%26dopt%3DAbstract</link>
            <description>Authors: Thorgersen EB, Ludviksen JK, Lambris JD, Sfyroera G, Nielsen EW, Mollnes TE
    C1-Inhibitor (C1-INH) is an important biological inhibitor, regulating several protein cascade systems. Recent research has shown that the molecule exhibits properties not dependent on its protease inhibition activity. Serum and whole blood from pigs and humans were pre-incubated with C1-INH, iC1-INH or the complement inhibitors SPICE or compstatin. Whole, live Escherichia coli were then added for further incubation. Complement activation, a range of cytokines, chemokines and growth factors, as well as the leukocyte activation markers wCD11R3 (pig) and CD11b (human) were measured. Both C1-INH and iC1-INH dose-dependently and significantly (P &amp;lt; 0.05) reduced a range of E. coli-induced pro-inflammator...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742902</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742902</guid>        </item>
        <item>
            <title>Evidence that a C1q/C1qR system regulates monocyte-derived dendritic cell differentiation at the interface of innate and acquired immunity.</title>
            <link>http://www.medworm.com/index.php?rid=2742901&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710097%26dopt%3DAbstract</link>
            <description>Authors: Hosszu KK, Santiago-Schwarz F, Peerschke EI, Ghebrehiwet B
    Growing evidence shows that C1q modulates the growth and function of cells committed to the monocyte-derived dendritic cell (DC) lineage. Because C1q regulates both innate and acquired immune responses, we postulated that C1q modulates the transition from monocytes to DCs, i.e. the interface between innate and acquired immunity. Human peripheral blood monocytes cultured with soluble C1q and DC growth factors (granulocyte-macrophage colony-stimulating factor + Interleukin-4) failed to down-regulate monocyte-associated (CD14, CD16) and up-regulate DC-associated (CD83, CD86) markers. Impaired DC differentiation was not due to apoptosis; further analysis revealed the development of CD14(hi)CD11c(hi)CD16 (+/-) cells that ha...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742901</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742901</guid>        </item>
        <item>
            <title>Enhanced Induction of a Histamine-Forming Enzyme, Histidine Decarboxylase, in Mice Primed With nod1 or nod2 Ligand in Response to Various Toll-Like Receptor Agonists.</title>
            <link>http://www.medworm.com/index.php?rid=2742900&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710098%26dopt%3DAbstract</link>
            <description>Authors: Funayama H, Huang L, Asada Y, Endo Y, Takada H
    We investigated the immunopharmacological aspects of innate immune responses via Toll-like receptors (TLRs), NOD1 and NOD2, in terms of induction of the histamine-forming enzyme, histidine decarboxylase (HDC), activity in mice. Intravenous injection of TLR4-agonistic synthetic lipid A definitely induced HDC activity in the liver, spleen, and lungs, especially the lungs, in mice, where maximum activity was induced about 3 h after the injection of lipid A. The TLR2/6 agonistic synthetic diacyl-type lipopeptide FSL-1 and TLR3-agonistic poly I:C were also effective in inducing HDC, while the NOD2-agonistic synthetic muramyldipeptide (MDP) and NOD1-agonistic synthetic FK156 and FK565 exhibited only weak activities in this respect. Mice...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742900</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742900</guid>        </item>
        <item>
            <title>Biofilm-forming Pseudomonas aeruginosa bacteria undergo lipopolysaccharide structural modifications and induce enhanced inflammatory cytokine response in human monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2742899&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710099%26dopt%3DAbstract</link>
            <description>Authors: Ciornei CD, Novikov A, Beloin C, Fitting C, Caroff M, Ghigo JM, Cavaillon JM, Adib-Conquy M
    To determine whether growth of bacteria in biofilms triggers a specific immune response, we compared cytokine induction in human monocytes and mouse macrophages by planktonic and biofilm bacteria. We compared Pseudomonas aeruginosa and Staphylococcus aureus, two bacteria often colonizing the airways of cystic fibrosis patients. Planktonic and biofilm S. aureus induced equivalent amounts of cytokine in human monocytes. In contrast, biofilm-forming P. aeruginosa induced a higher production of tumor necrosis factor and interleukin-6 than their planktonic counterpart, both for clinical isolates and laboratory strains. This increased cytokine production was partly dependent on phagocytosis. ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742899</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742899</guid>        </item>
        <item>
            <title>Expression of UDP-glucuronosyltransferase 1A6 isoform in Caco-2 cells stimulated with lipopolysaccharide.</title>
            <link>http://www.medworm.com/index.php?rid=2742898&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710100%26dopt%3DAbstract</link>
            <description>In this study, we investigated the in vitro effect of lipopolysaccharide (LPS) on the expression of the UGT1A6 isoform in human colon carcinoma Caco-2 cells. Results demonstrated a significant down-regulation of UGT1A6 expression, both in terms of mRNA and protein levels, and a reduced UGT activity after LPS exposure of cell cultures, suggesting a role for endotoxins on UGT regulation mechanisms.
    PMID: 19710100 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742898</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742898</guid>        </item>
        <item>
            <title>Influence of serum on the immune recognition of a synthetic lipopeptide mimetic of the 19-kDa lipoprotein from Mycobacterium tuberculosis.</title>
            <link>http://www.medworm.com/index.php?rid=2742897&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710101%26dopt%3DAbstract</link>
            <description>Authors: Schromm AB, Reiling N, Howe J, Wiesm&amp;#xFC;ller KH, Roessle M, Brandenburg K
    The innate immune response provides a critical first-line defense against Mycobacterium tuberculosis, an intracellular pathogen that represents a major health threat world-wide. A synthetic lipopeptide (LP) mimicking the lipid moiety of the cell-wall associated 19-kDa lipoprotein from M. tuberculosis has recently been assigned an important role in the induction of an antibacterial immune response in host macrophages. Here, we present experimental data on the biological activities and the biophysical mechanisms underlying cell activation by synthetic 19-kDa M. tuberculosis-derived lipopeptide (Mtb-LP). Investigation of the geometry of the LP (i.e. the molecular conformation and supramolecular aggregate ...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742897</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742897</guid>        </item>
        <item>
            <title>Lipopolysaccharide biosynthesis in Pseudomonas aeruginosa.</title>
            <link>http://www.medworm.com/index.php?rid=2742896&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710102%26dopt%3DAbstract</link>
            <description>Authors: King JD, Koc&amp;#xED;ncov&amp;#xE1; D, Westman EL, Lam JS
    Pseudomonas aeruginosa causes serious nosocomial infections, and an important virulence factor produced by this organism is lipopolysaccharide (LPS). This review summarizes knowledge about biosynthesis of all three structural domains of LPS - lipid A, core oligosaccharide, and O polysaccharides. In addition, based on similarities with other bacterial species, this review proposes new hypothetical pathways for unstudied steps in the biosynthesis of P. aeruginosa LPS. Lipid A biosynthesis is discussed in relation to Escherichia coli and Salmonella, and the biosyntheses of core sugar precursors and core oligosaccharide are summarised. Pseudomonas aeruginosa attaches a Common Polysaccharide Antigen and O-Specific Antigen polysacch...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742896</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742896</guid>        </item>
        <item>
            <title>Up-regulation of integrin expression in lung adenocarcinoma cells caused by bacterial infection: in vitro study.</title>
            <link>http://www.medworm.com/index.php?rid=2742895&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710103%26dopt%3DAbstract</link>
            <description>Authors: Gravelle S, Barnes R, Hawdon N, Shewchuk L, Eibl J, Lam JS, Ulanova M
    Integrins are a large family of adhesion receptors that are known to be key signaling molecules in both physiological and pathological processes. Previous studies have demonstrated that the expression of integrin receptors in the pulmonary epithelium can change under various pathological conditions, such as injury, inflammation, or malignant transformation. We hypothesize that integrin expression can be altered by stimulation of lung epithelial cells with an opportunistic bacterial pathogen Pseudomonas aeruginosa. Using the A549 adenocarcinoma cell line that expressed a low level of several integrin subunits we have demonstrated that P. aeruginosa infection in vitro caused a rapid up-regulation of alpha5, al...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742895</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742895</guid>        </item>
        <item>
            <title>Interleukin-6 is associated with liver lipid homeostasis but not with cell death in experimental hepatic steatosis.</title>
            <link>http://www.medworm.com/index.php?rid=2742894&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710104%26dopt%3DAbstract</link>
            <description>In conclusion, IL-6 ameliorated the mitochondria lipid disturbance in hepatocytes isolated from steatotic animals. Furthermore, PC is identified as a new survival agent that reverses several TNF-alpha-inducible responses that are likely to promote steatosis and necrosis.
    PMID: 19710104 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742894</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742894</guid>        </item>
        <item>
            <title>Regulation of Toll-like receptor 4-associated MD-2 in intestinal epithelial cells: a comprehensive analysis.</title>
            <link>http://www.medworm.com/index.php?rid=2742893&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19710105%26dopt%3DAbstract</link>
            <description>In this study, we did a comprehensive analysis to understand the immune-mediated and epigenetic mechanisms by which IECs down-regulate MD-2 expression. Expression of MD-2 and TLR4 mRNA was examined in human inflammatory bowel disease and intestinal epithelial cell lines (T84, HT-29, Caco-2). Nuclear factor-kappaB transcriptional activation was used as a measure of LPS responsiveness. Intestinal epithelial cells in patients with inflammatory bowel disease exhibited increased expression of MD-2 and TLR4 mRNA. Lipopolysaccharide responsiveness in IECs was polarized to the basolateral membrane. Bisulfite sequencing of the MD-2 promoter demonstrated methylation of CpG dinucleotides. Inhibition of methylation by 5-azacytidine and histone de-actylation by trichostatin A, two forms of epigenetic s...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742893</comments>
            <pubDate>Tue, 25 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742893</guid>        </item>
        <item>
            <title>Differential modulation of human B-defensins expression in human gingival epithelia by Porphyromonas gingivalis lipopolysaccharide with tetra- and penta-acylated lipid A structures.</title>
            <link>http://www.medworm.com/index.php?rid=2700241&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19675119%26dopt%3DAbstract</link>
            <description>This study suggests that P. gingivalis LPS with different lipid A structures could differentially modulate host innate immune responses in human gingival epithelia, which may be a hitherto undescribed novel pathogenic mechanism of P. gingivalis in periodontal pathogenesis.
    PMID: 19675119 [PubMed - as supplied by publisher] (Source: Innate Immunity)</description>
            <author>Innate Immunity</author>
            <type>journals</type>
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            <pubDate>Tue, 11 Aug 2009 23:00:00 +0100</pubDate>
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            <title>Altered innate immune response in farmers and smokers.</title>
            <link>http://www.medworm.com/index.php?rid=2700240&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19675120%26dopt%3DAbstract</link>
            <description>Authors: Sahlander K, Larsson K, Palmberg L
    Pig farmers and cigarette smokers are continuously exposed to pathogen-associated molecular patterns (PAMPs) have an increased prevalence of respiratory disorders, such as chronic bronchitis and chronic obstructive pulmonary decease (COPD). We hypothesized that markers of innate immunity, T-helper (Th) cell cytokine profile and acute responses to pro-inflammatory stimuli differ between smokers and farmers, who are exposed to organic material on a daily basis and healthy non-exposed subjects. Eleven non-smoking pig farmers, 12 non-farming smokers and 12 controls underwent bronchial lipopolysaccharide (LPS) challenge and exposure in a pig barn during 3 h on separate days. Toll-like receptor 2 (TLR2), TLR4 and CD14 on blood monocytes and neutrop...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2700240</comments>
            <pubDate>Tue, 11 Aug 2009 23:00:00 +0100</pubDate>
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            <title>Interleukin (IL)-10 attenuates lipopolysaccharide-induced IL-6 production via inhibition of I{kappa}B-{zeta} activity by Bcl-3.</title>
            <link>http://www.medworm.com/index.php?rid=2588823&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19586995%26dopt%3DAbstract</link>
            <description>Authors: Dagvadorj J, Naiki Y, Tumurkhuu G, Noman AS, Iftekar-E-Khuda I, Koide N, Komatsu T, Yoshida T, Yokochi T
    The inhibitory effect of interleukin-10 (IL-10), an anti-inflammatory cytokine, on lipopolysaccharide (LPS)-induced IL-6 production was characterized by simultaneous stimulation of RAW 264.7 cells with LPS and IL-10. The presence of IL-10 significantly inhibited LPS-induced IL-6 production at a transcriptional level. The expression of IkappaB-zeta, which promotes IL-6 production, was induced in response to LPS and it was definitely suppressed in the presence of IL-10. Further, IL-10 inhibited LPS-induced NF-kappaB activation. A pharmacological inhibitor of NF-kappaB prevented LPS-induced IkappaB-zeta expression, suggesting that IL-10 might inhibit LPS-induced IkappaB-zeta e...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
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            <pubDate>Tue, 07 Jul 2009 23:00:00 +0100</pubDate>
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            <title>TLR4-mediated induction of TLR2 signaling is critical in the pathogenesis and resolution of otitis media.</title>
            <link>http://www.medworm.com/index.php?rid=2588822&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19586996%26dopt%3DAbstract</link>
            <description>Authors: Leichtle A, Hernandez M, Pak K, Yamasaki K, Cheng CF, Webster NJ, Ryan AF, Wasserman SI
    Otitis media is the most prevalent childhood disease in developed countries. The involvement of Toll-like receptors (TLRs) in otitis media pathophysiology has been implicated by studies in cell lines and association studies of TLR gene polymorphisms. However, precise functions of TLRs in the etiology of otitis media in vivo have not been examined. We investigated the inflammatory response to nontypeable Haemophilus influenzae using a model of otitis media in wild-type, TLR2(-/-) and TLR4(-/-) mice by gene microarray, qPCR, immunohistochemistry, Western blot analysis and histopathology. Toll-like receptor-2(-/-) and TLR4(-/-) mice exhibited a more profound, persistent inflammation with impai...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
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            <pubDate>Tue, 07 Jul 2009 23:00:00 +0100</pubDate>
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            <title>Detection and quantification of five major periodontal pathogens by single copy gene-based real-time PCR.</title>
            <link>http://www.medworm.com/index.php?rid=2588821&amp;cid=s_37090_3_f&amp;fid=37090&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19586997%26dopt%3DAbstract</link>
            <description>Authors: Hyv&amp;#xE4;rinen K, Laitinen S, Paju S, Hakala A, Suominen-Taipale L, Skurnik M, K&amp;#xF6;n&amp;#xF6;nen E, Pussinen PJ
    Periodontitis is a common chronic multibacterial infection in the tooth-supporting tissues. It has been shown that periodontitis patients carry higher number of disease-associated bacteria than healthy ones. The aim of this study was to generate a novel, single copy gene-based quantitative real-time PCR (qPCR) assay for five major periodontal pathogens - Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Treponema denticola, and Tannerella forsythia. The primer/probe sets were designed for conservative lipopolysaccharide-coding gene regions. They proved to be sensitive and able to detect strains representing different serotypes of...</description>
            <author>Innate Immunity</author>
            <type>journals</type>
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            <pubDate>Tue, 07 Jul 2009 23:00:00 +0100</pubDate>
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