Interplay between oxidative stress and immunity in the progression of alcohol-mediated liver injury.
Inflammation is recognized increasingly as having an important role in the pathogenesis of alcoholic liver disease (ALD). Nonetheless, the mechanisms by which alcohol maintains hepatic inflammation are still characterized incompletely. Several studies have demonstrated that ethanol-induced oxidative stress promotes immune responses in ALD by stimulating both humoral and cellular reactions against liver proteins adducted to hydroxyethyl free radicals and several lipid peroxidation products. Moreover, ALD patients have autoantibodies targeting cytochrome P4502E1 and oxidized phospholipids. In both chronic alcohol-fed rats and heavy drinkers, the elevation of IgG against lipid peroxidation-derived antigens is associated with tumor necrosis factor-alpha production and the severity of liver inflammation. On this basis, we propose that allo- and autoimmune reactions associated with oxidative stress might contribute to fueling hepatic inflammation in ALD.
Vidali
Matteo
M
Department of Medical Sciences and Interdepartmental Research Centre for Autoimmune Diseases, University Amedeo Avogadro of East Piedmont, Novara, Italy.
Stewart
Stephen F
SF
Albano
Emanuele
E
D000428:Alcohol Drinking / Q000009:adverse effects; D000818:Animals; D018450:Disease Progression; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D008108:Liver Diseases, Alcoholic / Q000276:immunology* / Q000378:metabolism; D008954:Models, Biological; D018384:Oxidative Stress / Q000276:immunology*; D051381:Rats
D005609:Free Radicals; D007074:Immunoglobulin G