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Interleukin-33 overexpression is associated with liver fibrosis in mice and humans.

Abstract : Interleukin-33 (IL-33), the most recently identified member of the IL-1 family, induces synthesis of T Helper 2 (Th2)-type cytokines via its heterodimeric ST2/IL-1RAcP receptor. Th2-type cytokines play an important role in fibrosis; thus, we investigated the role of IL-33 in liver fibrosis. IL-33, ST2 and IL-1RAcP gene expression was analysed in mouse and human normal (n= 6) and fibrotic livers (n= 28), and in human hepatocellular carcinoma (HCC; n= 22), using real-time PCR. IL-33 protein was detected in normal and fibrotic liver sections and in isolated liver cells using Western blotting and immunolocalization approaches. Our results showed that IL-33 and ST2 mRNA was overproduced in mouse and human fibrotic livers, but not in human HCC. IL-33 expression correlated with ST2 expression and also with collagen expression in fibrotic livers. The major sources of IL-33 in normal liver from both mice and human beings are the liver sinusoidal endothelial cells and, in fibrotic liver, the activated hepatic stellate cells (HSC). Moreover, IL-33 expression was increased in cultured HSC when stimulated by pro-inflammatory cytokines. In conclusion, IL-33 is strongly associated with fibrosis in chronic liver injury and activated HSC are a source of IL-33.
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https://hal.archives-ouvertes.fr/hal-00660257
Contributor : Alice Brébion <>
Submitted on : Monday, January 16, 2012 - 11:50:29 AM
Last modification on : Thursday, January 14, 2021 - 11:19:47 AM

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Pierrick Marvie, Mariette Lisbonne, Annie l'Helgoualc'H, Michel Rauch, Bruno Turlin, et al.. Interleukin-33 overexpression is associated with liver fibrosis in mice and humans.. Journal of Cellular and Molecular Medicine, Wiley Open Access, 2010, 14 (6B), pp.1726-39. ⟨10.1111/j.1582-4934.2009.00801.x⟩. ⟨hal-00660257⟩

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