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<title lang=en>Endogenous IL-33 Deficiency Exacerbates Liver Injury and Increases Hepatic Influx of Neutrophils in Acute Murine Viral Hepatitis</title>
<creator>Carrière, Virginie</creator>
<creator>Arshad, Muhammad Imran</creator>
<creator>Le Seyec, Jacques</creator>
<creator>Lefèvre, Benjamin</creator>
<creator>Farooq, Muhammad</creator>
<creator>Jan, Aurélien</creator>
<creator>Manuel, Christelle</creator>
<creator>Touami-Bernard, Laurence</creator>
<creator>Lucas-Clerc, Catherine</creator>
<creator>Genet, Valentine</creator>
<creator>Gascan, Hugues</creator>
<creator>Girard, Jean-Philippe</creator>
<creator>Chalmel, Frédéric</creator>
<creator>Lamontagne, Lucie</creator>
<creator>Piquet-Pellorce, Claire</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>Laboratoire de biochimie générale ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>Institut de Génétique et Développement de Rennes (IGDR) ; Université de Rennes 1 (UR1) - Centre National de la Recherche Scientifique (CNRS) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Institut de pharmacologie et de biologie structurale (IPBS) ; Université Paul Sabatier - Toulouse 3 (UPS) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Département des Sciences Biologiques [Montréal] ; Université du Québec à Montréal (UQAM)</contributor>
<contributor>This work was supported by INSERM and the University of Rennes 1, the “Contrat de Projet Etat Région” CPER Infectio 2016-2022. The authors would like to thank the H2P2 platform for immunohistochemistry analysis and the BIOSIT technological platform for flow cytometry analysis and animal house facilities. Muhammad Imran Arshad has been supported by a research grant funded by Higher Education Commission under NRPU (Project no. 20-4613/NRPU/R&D/HEC/14/45) scheme at the University of Agriculture, Faisalabad, Pakistan. Muhammad Farooq was supported by a Ph.D. fellowship from the Government of Pakistan (Higher Education Commission, University of Veterinary and Animal Sciences, Lahore). Virginie Carrière has been supported by Fondation de la Recherche Médicale (FRM), France.</contributor>
<description>International audience</description>
<source>Mediators of Inflammation</source>
<identifier>hal-01544268</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01544268</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01544268</source>
<source>Mediators of Inflammation, 2017, 2017, pp.1359064. 〈10.1155/2017/1359064〉</source>
<identifier>DOI : 10.1155/2017/1359064</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1155/2017/1359064</relation>
<identifier>PUBMED : 28607531</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/28607531</relation>
<identifier>PUBMEDCENTRAL : PMC5457781</identifier>
<language>en</language>
<subject>[SDV.GEN] Life Sciences [q-bio]/Genetics</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>The alarmin IL-33 has been described to be upregulated in human and murine viral hepatitis. However, the role of endogenous IL-33 in viral hepatitis remains obscure. We aimed to decipher its function by infecting IL-33-deficient mice (IL-33 KO) and their wild-type (WT) littermates with pathogenic mouse hepatitis virus (L2-MHV3). The IL-33 KO mice were more sensitive to L2-MHV3 infection exhibiting higher levels of AST/ALT, higher tissue damage, significant weight loss, and earlier death. An increased depletion of B and T lymphocytes, NKT cells, dendritic cells, and macrophages was observed 48 h postinfection (PI) in IL-33 KO mice than that in WT mice. In contrast, a massive influx of neutrophils was observed in IL-33 KO mice at 48 h PI. A transcriptomic study of inflammatory and cell-signaling genes revealed the overexpression of IL-6, TNFα, and several chemokines involved in recruitment/activation of neutrophils (CXCL2, CXCL5, CCL2, and CCL6) at 72 h PI in IL-33 KO mice. However, the IFNγ was strongly induced in WT mice with less profound expression in IL-33 KO mice demonstrating that endogenous IL-33 regulated IFNγ expression during L2-MHV3 hepatitis. In conclusion, we demonstrated that endogenous IL-33 had multifaceted immunoregulatory effect during viral hepatitis via induction of IFNγ, survival effect on immune cells, and infiltration of neutrophils in the liver.</description>
<date>2017</date>
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