Priority Research Papers:

Endogenous IL-33 has no effect on the progression of fibrosis during experimental steatohepatitis

Philippe Vasseur, Sarah Dion, Aveline Filliol, Valentine Genet, Catherine Lucas-Clerc, Girard Jean-Philippe, Christine Silvain, Jean-Claude Lecron, Claire Piquet-Pellorce and Michel Samson _

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Oncotarget. 2017; 8:48563-48574. https://doi.org/10.18632/oncotarget.18335

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Philippe Vasseur1,2,*, Sarah Dion3,*, Aveline Filliol3, Valentine Genet3, Catherine Lucas-Clerc4, Girard Jean-Philippe5, Christine Silvain2,6, Jean-Claude Lecron2,7, Claire Piquet-Pellorce3 and Michel Samson3

1 Service d’Hépato-Gastroentérologie, Centre Hospitalier Nord Deux-Sèvres, Thouars, France

2 Laboratoire Inflammation Tissus Epithéliaux et Cytokines, Université de Poitiers, Poitiers, France

3 Institut National de la Santé et de la Recherche Médicale, Institut de Recherche Santé Environnement & Travail, Université de Rennes, Rennes, France

4 Service de Biochimie, Centre Hospitalier Universitaire, Rennes, Université de Rennes, Rennes, France

5 Institut de Pharmacologie et de Biologie Structurale, Centre National de la Recherche Scientifique, Université de Toulouse, Toulouse, France

6 Service d’Hépato-Gastroentérologie, Centre Hospitalier Universitaire de Poitiers, Poitiers, France

7 Service d’Immunologie et Inflammation, Centre Hospitalier Universitaire de Poitiers, Poitiers, France

* These authors have contributed equally to this work

Correspondence to:

Michel Samson, email:

Keywords: nonalcoholic steatohepatitis, NASH, nonalcoholic fatty liver disease, NAFLD, immune cells

Received: December 20, 2016 Accepted: May 15, 2017 Published: June 01, 2017


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 IL-33-/—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.

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