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Interleukin (IL) -35 is an anti-inflammatory cytokine which exerts various beneficial effects on autoimmune diseases. However, whether IL-35 plays a role in endotoxin induced hepatitis demands clarification. This study aims to reveal the effect and mechanism of IL-35 on endotoxin induced liver injury. Acute hepatic injury was induced by  D -galactosamine ( D -GalN, 400 mg/kg) and lipopolysaccharide (LPS, 5 μg/kg) administration in mice. IL-35 treatment ameliorated  D -GalN/LPS induced liver injury in a dose dependent manner as shown by histological examination, ALT determination and Caspase-3 activity assay. It also reduced production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, IL-1β, and IL-6, and increased production of anti-inflammatory cytokines, IL-4, IL-10, and transforming growth factor (TGF)-β. This hepato-protective effect was proved mainly mediated by Kupffer cells (KC) via gadolinium chloride depletion and cell adoptive transfer experiment. In addition, IL-35 emolliated the cytotoxicity of LPS-triggered KCs to hepatocytes, suppressed nitric oxide (NO) and TNF-α production, and elevated IL-10 production in LPS stimulated KCs. Furthermore, IL-35 could not exert hepato-protective effect in IL-10-deficient mice  in vivo  and it could not suppress LPS induced NO and TNF-α production in IL-10-deficient KCs  in vitro . In conclusion, IL-35 protects endotoxin-induced acute liver injury, which mainly acts thought increasing IL-10 production in KCs. This finding demonstrates a role of IL-35 in anti-infectious immunity and provides a potential therapeutic target in treating fulminant hepatitis.

Interleukin-35 Attenuates D-Galactosamine/Lipopolysaccharide-Induced Liver Injury via Enhancing Interleukin-10 Production in Kupffer Cells