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<title lang=en>Endogenous IL-33 has no effect on the progression of fibrosis during experimental steatohepatitis</title>
<creator>Vasseur, Philippe</creator>
<creator>Dion, Sarah</creator>
<creator>Filliol, Aveline</creator>
<creator>Genet, Valentine</creator>
<creator>Lucas-Clerc, Catherine</creator>
<creator>Girard, Jean-Philippe</creator>
<creator>Silvain, Christine</creator>
<creator>Lecron, Jean-Claude</creator>
<creator>Piquet-Pellorce, Claire</creator>
<creator>Samson, Michel</creator>
<contributor>Laboratoire Inflammation, tissus épithéliaux et cytokines (LITEC) ; Université de Poitiers</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>Laboratoire de biochimie générale ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</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>Hôpital de la Milétrie ; CHU de Poitiers</contributor>
<contributor>INSERM</contributor>
<contributor> Ministere de l'Education Nationale de la Recherche et de la Technologie</contributor>
<contributor> University of Rennes 1</contributor>
<contributor> Region Bretagne</contributor>
<contributor> Ligue contre le cancer, comites du grand Ouest</contributor>
<description>International audience</description>
<source>ISSN: 1949-2553</source>
<source>Oncotarget</source>
<publisher>Impact journals</publisher>
<identifier>hal-01578584</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01578584</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01578584</source>
<source>Oncotarget, Impact journals, 2017, 8 (30), pp.48563--48574. 〈10.18632/oncotarget.18335〉</source>
<identifier>DOI : 10.18632/oncotarget.18335</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.18632/oncotarget.18335</relation>
<identifier>PUBMED : 28611297</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/28611297</relation>
<language>en</language>
<subject lang=en>nonalcoholic steatohepatitis</subject>
<subject lang=en> nash</subject>
<subject lang=en> nonalcoholic fatty liver disease</subject>
<subject lang=en> nafld</subject>
<subject lang=en> immune cells</subject>
<subject>[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Interleukin (IL)-33 has been recently reported to be strongly pro-fibrogenic in various models of liver disease. Our aim was to study the role of endogenous IL-33 in a diet-induced model of steatohepatitis. IL-33 deficient mice and wild type (WT) littermates received a high-fat diet (HFD), or a standard diet for 12 weeks. The HFD-induced steatohepatitis was associated with an upregulation of IL-33 transcripts and protein. An insulin tolerance test revealed lower systemic insulin sensitivity in IL33-/-HFD mice than in WT-HFD mice. Nevertheless, IL-33 deficiency did not affect the severity of liver inflammation by histological and transcriptomic analyses, nor the quantity of liver fibrosis. Livers from HFD mice had more myeloid populations, markedly fewer NKT cells and higher proportion of ST2+ Treg cells and ST2+ type 2 innate lymphoid cells (ILC2), all unaffected by IL-33 deficiency. In conclusion, deficiency of endogenous IL-33 does not affect the evolution of experimental diet-induced steatohepatitis towards liver fibrosis.</description>
<date>2017</date>
</dc>
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