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Alcohol, injury, and cellular immunity

Journal

ALCOHOL
Volume 28, Issue 3, Pages 137-149

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/S0741-8329(02)00278-1

Keywords

ethanol; trauma; burn injury; cytokines; interleukins; immune responses

Funding

  1. NIAAA NIH HHS [AA12034-S1, AA12034] Funding Source: Medline

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It is widely accepted that alcohol exposure is a causative factor in the occurrence of burn or other traumatic injury. It is less well known that individuals who have consumed alcohol before sustaining an injury suffer from increased morbidity and mortality compared with the morbidity and mortality of non-alcohol-consuming subjects with similar injuries. Complications due to bacterial infection are the most common burn sequelae in injured patients and are frequently associated with depressed immunity. Independently, alcohol exposure and injury have been shown to influence cellular immunity negatively. These changes in immunity are closely linked to injury- or alcohol-induced alterations in the cytokine milieu in both clinical studies and animal models. Not surprisingly, the combination of insult of alcohol exposure and burn injury results in immune suppression that is greater in magnitude and duration compared with either insult alone. The combined effects of alcohol and injury on immunity have been examined in a limited number of studies. However, results of these studies support the suggestion that altered cytokine production is an integral part of the immune dysregulation and increased mortality that is observed. In particular, the increased presence of macrophage-derived mediators observed after burn or alcohol exposure alone seems to be synergistically increased in a combined injury model. Although more research is needed, it is likely that therapeutic modalities that include manipulation of cytokine networks to boost cellular immunity may improve outcome for patients who sustain injuries subsequent to consuming alcohol. (C) 2002 Elsevier Science Inc. All rights reserved.

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