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Immune dysfunction in acute alcoholic hepatitis

World Journal of Gastroenterology 2015年第42期21卷 11904-11913页

作者： Ashwin D Dhanda Peter l Collins School of Clinical Sciences University of Bristol NIHR Academic Clinical lecturer in Hepatology Institute of Translational and Stratified Medicine Plymouth University Peninsula Schools of Medicine and Dentistry South West liver Unit Plymouth Hospitals NHS Trust Department of liver Medicine University Hospitals Bristol NHS Foundation Trust

Acute alcoholic hepatitis(AAH) is a serious complication of alcohol misuse and has high short term mortality. It is a clinical syndrome characterised by jaundice and coagulopathy in a patient with a history of recent heavy alcohol use and is associated with profound immune dysfunction with a primed but ineffective immune response against pathogens. Here, we review the current knowledge of the pathogenesis and immune defects of AAH and identify areas requiring further study. Alcohol activates the immune system primarily through the disruption of gut tight junction integrity allowing the escape of pathogenassociated molecular particles(PAMPs) into the portal venous system. PAMPs stimulate cells expressing toll-like receptors(mainly myeloid derived cells) and initiate a network of intercellular signalling by secretion of many soluble mediators including cytokines and chemokines. The latter coordinates the infiltration of neutrophils, monocytes and T cells and results in hepatic stellate cell activation, cellular damage and hepatocyte death by necrosis or apoptosis. On the converse of this immune activation is the growing evidence of impaired microbial defence. Neutrophils have reduced phagocytic capacity and oxidative burst and there is recent evidence that T cell exhaustion plays a role in this.

关键词： Alcoholic hepatitis Alcoholic liver disease toll-l

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