Alcoholic hepatitis (AH) is a clinical syndrome characterized by
jaundice and progressive inflammatory liver injury in patients with a history of prolonged periods of excess alcohol consumption and recent heavy
alcohol abuse. Severe AH is a life-threatening form of alcohol-associated
liver disease with a high short-term mortality rate around 30-50% at one month from the initial presentation. A large number of pro-inflammatory mediators, metabolic pathways, transcriptional factors and epigenetic factors have been suggested to be associated with the development and progression of AH. Several factors may contribute to
liver failure and mortality in patients with severe AH including hepatocyte death,
inflammation, and impaired liver regeneration. Although the pathogeneses of AH have been extensively investigated and many therapeutic targets have been identified over the last five decades, no new drugs for AH have been successfully developed. In this review, we discuss
interleukin-22 (IL-22) biology and its roles of anti-apoptosis, anti-
fibrosis, anti-oxidation, anti-
bacterial infection and regenerative stimulation in protecting against liver injury in many preclinical models including several recently developed models such as chronic-plus-binge
ethanol feeding,
acute-on-chronic liver failure, C-X-C motif
chemokine ligand 1 plus high-fat diet-induced
nonalcoholic steatohepatitis. Finally, clinical trials of
IL-22 for the treatment of AH are also discussed, which showed some promising benefits for AH patients.