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<title lang=en>Pathogenic Mouse Hepatitis Virus or Poly(I:C) Induce IL-33 in Hepatocytes in Murine Models of Hepatitis.</title>
<creator>Arshad, Muhammad Imran</creator>
<creator>Patrat-Delon, Solène</creator>
<creator>Piquet-Pellorce, Claire</creator>
<creator>L'Helgoualc'H, Annie</creator>
<creator>Rauch, Michel</creator>
<creator>Genet, Valentine</creator>
<creator>Lucas-Clerc, Catherine</creator>
<creator>Bleau, Christian</creator>
<creator>Lamontagne, Lucie</creator>
<creator>Samson, Michel</creator>
<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>Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Laboratoire de biochimie générale ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>Département des Sciences Biologiques [Montréal] ; Université du Québec à Montréal (UQAM)</contributor>
<description>International audience</description>
<source>ISSN: 1932-6203</source>
<source>PLoS ONE</source>
<publisher>Public Library of Science</publisher>
<identifier>hal-00874120</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00874120</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00874120/document</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00874120/file/Pathogenic_Mouse_Hepatitis-accepted.pdf</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00874120</source>
<source>PLoS ONE, Public Library of Science, 2013, 8 (9), pp.e74278. 〈10.1371/journal.pone.0074278〉</source>
<identifier>DOI : 10.1371/journal.pone.0074278</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0074278</relation>
<identifier>PUBMED : 24058536</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/24058536</relation>
<language>en</language>
<subject>[SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>The IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33.</description>
<date>2013</date>
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