Alcoholic Liver Disease And Immune Response

ABSTRACT

The alcoholic liver disease (ALD) continues to be a major health problem worldwide with respect to both mor-bidity and mortality. It is usually an outcome of excessive alcohol consumptions but can be worse by poor diet and genetic factors. This review aims to update the recent conditions of the epidemiology, pathogenesis, immune response and thera-pies to ALD. The new insights into the pathogenesis of ALD include the key roles of the excess production of cytokines, reactive oxygen species (ROS) and the shortage of protective mediators, including adiponectin. As the liver injury pro-gresses, the immune system fails to counteract proinflammatory cytokines and ROS which further cause oxidative liver injury. By inducing mitochondrial alterations, oxidative stress promotes hepatocyte necrosis, release of pro-fibrotic cyto-kines and activation of collagen gene expression in hepatic stellate cells contributing to alcohol induced sensitization of hepatocyte to pro-apoptotic action of TNF-α. ALD can progress to cirrhosis, hepatocellular carcinoma, and liver failure. Regulation of perioxisome proliferator activated receptor (PPAR) and sterol regulatory element binding protein (SREBP) accompanied with lifestyle modifications are currently in practice for alleviating ALD.

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