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*ETHANOL
The Journal of Immunology, 1999, 162: 7441-7445.
Copyright © 1999 by The American Association of Immunologists

Alcohol (Ethanol) Inhibits IL-8 and TNF: Role of the p38 Pathway1

Saman Arbabi2, Iris Garcia, Gregory J. Bauer and Ronald V. Maier

Department of Surgery, University of Washington School of Medicine, Seattle, WA 98195

Acute ethanol (EtOH) intoxication has been identified as a risk factor for infectious complications in trauma and burn victims. However, the mechanism of this immune dysfunction has yet to be elucidated. The monocyte/macrophage production of cytokines, in particular IL-8 and TNF-{alpha}, is critical in the regulation of the acute inflammatory response to infectious challenge. IL-8 is a potent chemoattractant and activator of neutrophils. TNF-{alpha}, a proinflammatory cytokine, initiates expression of endothelial cell surface adhesion molecules and neutrophil migration. p38, a member of the mitogen-activated protein kinases, plays an important role in mediating intracellular signal transduction in endotoxin-induced inflammatory responses. We examined the effects of LPS and ethanol on p38 activation and the corresponding IL-8 and TNF-{alpha} production in human mononuclear cells. LPS-induced IL-8 and TNF-{alpha} production was inhibited in a similar pattern by pretreatment with either EtOH or SB202190 (1 µM), a specific inhibitor of p38 kinase. Western blot analysis, using a dual phospho-specific p38 mitogen-activated protein kinase Ab, demonstrated that EtOH pretreatment inhibited LPS-induced p38 activation. These results demonstrate that alcohol suppresses the normal host immune inflammatory response to LPS. This dysregulation appears to be mediated in part via inhibition of p38 activation. Inhibition of IL-8 and TNF-{alpha} production by acute EtOH intoxication may inhibit inflammatory focused neutrophil migration and activation and may be a mechanism explaining the increased risk of trauma- and burn-related infections.




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