Acute alcohol consumption alters the peripheral cytokines IL-8 and TNF-α.

Abstract

Acute alcohol consumption triggers release of cytokines, which are immune signaling molecules. Dysregulated cytokine levels are associated with impaired immune function, and peripheral cytokine levels may communicate with the brain to propagate drinking-related behaviors. This exploratory study aims to characterize the peripheral cytokine response to an alcohol challenge in a well-controlled laboratory setting. Moderate alcohol drinkers (n=17), abstinent for >5 days, consumed alcohol calibrated to achieve blood concentrations of 120mg/dL. Serum cytokine levels (IL-6, IL-8, IL-12, IFN-γ, TNF-α) were measured prior to drinking, 6h after drinking, and 24h after drinking. Linear mixed models evaluated within-subject differences in cytokine levels over time. The pro-inflammatory chemokine IL-8 significantly increased 6h after alcohol [F(1,34)=4.13, p=0.0002, d'=0.5]. In contrast, the pro-inflammatory cytokine TNF-α significantly decreased 6h after alcohol [F(1,34)=-3.07, p=0.004, d'=0.3]. No cytokines were significantly different from baseline 24h after alcohol. In our exploratory data, acute alcohol challenge (120mg/dL) elicits dynamic changes in the pro-inflammatory molecules IL-8 and TNF-α. The findings help inform the temporal profile of cytokine response to alcohol, and identify IL-8 as a cytokine of interest for future studies of periphery-brain immune communication.