Inflammation is commonly observed in
liver diseases and is frequently complicated by
fibrosis and
cirrhosis in end-stage disease. The only curative treatment for cirrhotic patients is
liver transplantation. However, organ shortage as well as an increasing organ demand call for early treatment of
liver disease and prevention of
fibrosis. Experimental data have shown the critical role of pro-inflammatory
cytokines like
tumor necrosis factor-alpha (
TNF-alpha) and
interferon-gamma (IFN-gamma) in the development of liver injury. Here, we review our work on the role of endogenously produced
interleukin-10 (IL-10), a potent anti-inflammatory
cytokine, in several experimental models of acute and chronic liver injury. First, in acute macrophage-mediated
hepatitis induced by
galactosamine/
lipopolysaccharide administration,
IL-10 neutralisation led to a more severe liver damage, whereas
IL-10 injection, even delayed, was able to limit liver
necrosis. A similar protective effect of
IL-10 was observed in acute T cell-mediated
hepatitis induced by
concanavalin A (Con A) injection. The immunoregulatory role of
IL-10 was then established after repeated exposition to Con A. In
carbon tetrachloride liver injury, two other properties of
IL-10 have been suggested: modulation of hepatocyte proliferation and modulation of
liver fibrosis. Finally, the potential therapeutic applications in human
liver disease as well as the potential side effects are discussed.