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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-15T18:21:15Z</responseDate> <request identifier=oai:HAL:hal-01373946v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-01373946v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:IRSET-HIAEC</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:GIP-BE</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:INSERM</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:IRSET-2</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>Toll-like receptor-2 exacerbates murine acute viral hepatitis</title> <creator>Bleau, C.</creator> <creator>Burnette, M.</creator> <creator>Filliol, Aveline</creator> <creator>Piquet-Pellorce, Claire</creator> <creator>Samson, Michel</creator> <creator>Lamontagne, Lucie</creator> <contributor>Département des Sciences Biologiques [Montréal] ; Université du Québec à Montréal (UQAM)</contributor> <contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>2895-2009, NSERC, Natural Sciences and Engineering Research Council of Canada</contributor> <description>International audience</description> <source>Immunology</source> <identifier>hal-01373946</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01373946</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01373946/document</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01373946/file/Toll-like%20receptor%20%28tlr%29-2%20exacerbates%20murine%20acute%20viral%20hepatitis.pdf</identifier> <source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01373946</source> <source>Immunology, 2016, 149, pp.204--224. 〈10.1111/imm.12627〉</source> <identifier>DOI : 10.1111/imm.12627</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1111/imm.12627</relation> <identifier>PUBMED : 27273587</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/27273587</relation> <language>en</language> <subject lang=en>Toll-like receptor-2</subject> <subject lang=en> coronavirus</subject> <subject lang=en> inflammation</subject> <subject lang=en> viral hepatitis</subject> <subject>[SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health</subject> <subject>[SDV.IMM] Life Sciences [q-bio]/Immunology</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Viral replication in the liver is generally detected by cellular endosomal Toll-like receptors (TLRs) and cytosolic helicase sensors that trigger antiviral inflammatory responses. Recent evidence suggests that surface TLR2 may also contribute to viral detection through recognition of viral coat proteins but its role in the outcome of acute viral infection remains elusive. In this study, we examined in vivo the role of TLR2 in acute infections induced by the highly hepatotrophic mouse hepatitis virus (MHV) type 3 and weakly hepatotrophic MHV-A59 serotype. To address this, C57BL/6 (wild-type; WT) and TLR2 knockout (KO) groups of mice were intraperitoneally infected with MHV3 or MHV-A59. MHV3 infection provoked a fulminant hepatitis in WT mice, characterized by early mortality and high alanine and aspartate transaminase levels, histopathological lesions and viral replication whereas infection of TLR2 KO mice was markedly less severe. MHV-A59 provoked a comparable mild and subclinical hepatitis in WT and TLR2 KO mice. MHV3-induced fulminant hepatitis in WT mice correlated with higher hepatic expression of interferon-β, interleukin-6, tumour necrosis factor-α, CXCL1, CCL2, CXCL10 and alarmin (interleukin-33) than in MHV-A59-infected WT mice and in MHV3-infected TLR2 KO mice. Intrahepatic recruited neutrophils, natural killer cells, natural killer T cells or macrophages rapidly decreased in MHV3-infected WT mice whereas they were sustained in MHV-A59-infected WT mice and MHV3-infected TLR2 KO. MHV3 in vitro infection of macrophagic cells induced rapid and higher viral replication and/or interleukin-6 induction in comparison to MHV-A59, and depended on viral activation of TLR2 and p38 mitogen-activated protein kinase. Taken together, these results support a new aggravating inflammatory role for TLR2 in MHV3-induced acute fulminant hepatitis. © 2016 John Wiley & Sons Ltd</description> <date>2016</date> <rights>info:eu-repo/semantics/OpenAccess</rights> </dc> </metadata> </record> </GetRecord> </OAI-PMH>