Journal of Liver

Dual face functional role of IL-33 during immune cell mediated and hepato-toxic induced acute liver injury

World Congress on Hepatitis

July 20-22, 2015 Orlando, Florida, USA

Michel Samson

Posters-Accepted Abstracts: J Liver

Abstract:

IL-33/ST2 axis play a protective role during acute hepatitis but little is known about the functional role of endogenous IL-33 in liver patho-physiology. We aimed to decipher the functional role of IL-33 by using IL-33 deficient mice during immune cell mediated and hepatotoxic driven liver injury. We used a genetic model of acute hepatitis by using IL-33 deficient mice in ConA (a T cell-mediated hepatitis) and CCl4 (a hepatotoxic agent-induced hepatitis) induced acute liver injury. The liver functions (AST/ALT), signature of cytokines and characterization of infiltrate cell in WT and IL-33-/-mice were carried out by biochemistry, qPCR and flow cytometry analyses. Our results demonstrated that IL-33-/- mice exhibited more severe ConA liver injury than WT mice evidencing a protective effect of IL-33 in this hepatic model while no difference was observed in CCl4-hepatitis between WT and IL-33-/- mice. The ConA-induced hepatic injury was associated with increased TNF-?, IL-1-?, IFN-? and IL-6 cytokines in WT and IL-33-/- mice. The level of TNF-? and IL-1-? but not of IFN-? and IL-6 was significantly higher in IL-33-/- mice than WT control. The intra-hepatic percentage of NK, NKT cells, T cells and B cells was not altered significantly between WT and IL-33-/- mice following ConA-hepatitis. In conclusion, we evidenced that the genetic ablation of IL-33 sensitized the mice to severe ConA liver injury but not CCl4-mediated liver injury. IL-33 has a limited impact on pro-inflammatory cytokines and influx of infiltrate cells during immune cell mediated liver pathology.