Consequences of alcohol consumption on host defence.
This communication reviews recent literature and summarizes current views on the immunomodulatory effects of acute and chronic alcohol consumption. Chronic and even acute, moderate alcohol use can increase host susceptibility to infections caused by bacterial and viral pathogens. Impaired host defence after alcohol exposure appears to be linked to a combination of decreased inflammatory response, altered cytokine production, and abnormal reactive oxygen intermediate generation. Furthermore, cellular immunity, particularly antigen-specific immune response, is impaired by both acute and chronic alcohol use. Although T lymphocyte functions can be directly affected by ethanol, decreased antigen presenting cell function appears to be a key element in the ethanol-induced decrease in cell-mediated immunity. In addition, a preferential induction of Th2 vs Th1 immune response has been suggested, based on the increased immunoglobulin levels seen in chronic alcoholics. The effects of chronic and acute alcohol consumption in humans, animal models and in vitro systems on host defence and immunity are discussed in the context of the functional abnormalities of T and B lymphocytes, natural killer cells and monocytes/macrophages resulting in the altered immune response seen after alcohol use.
Szabo
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Department of Medicine, University of Massachusetts Medical Center, Worcester 01655, USA.
D000428:Alcohol Drinking / Q000009:adverse effects / Q000276:immunology*; D000437:Alcoholism / Q000276:immunology*; D016207:Cytokines / Q000097:blood; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects / Q000276:immunology; D007111:Immunity, Cellular / Q000187:drug effects / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood; D017382:Reactive Oxygen Species / Q000378:metabolism
D016207:Cytokines; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species