Influence of Chronic Dietary Ethanol on Cytokine Production by Murine Splenocytes and Thymocytes

Prolonged consumption of ethanol (ETOH) results in alterations of host defense via immune modulation, increasing susceptibility to infection. In the present study, effects of chronic dietary ETOH on cytokine production by splenocytes and thymocytes, splenocyte and thymocyte proliferation induced by mitogens, splenic natural killer cell activity, and antibody production (IgA and IgG) were examined. C57BL/6 mice were fed 5% ETOH v/v in the Lieber‐DeCarli liquid diet for 11 weeks. Release of interleukin (IL)‐2, IL‐5, IL‐6, IL‐10, and interferon (IFN)‐γ produced by concanavalin A (Con A) stimulated splenocytes was significantly decreased, whereas secretion of IL‐4 was slightly decreased by chronic dietary ETOH compared with controls. Production of tumor necrosis factor‐α and IL‐6 by lipopolysaccharide‐stimulated splenocytes was significantly and slightly decreased by ETOH compared with controls, respectively. Splenocyte and thymocyte proliferation induced by Con A was significantly inhibited by ETOH, whereas splenocyte proliferation induced by lipopolysaccharide was not affected. Natural killer cell activity was significantly inhibited by ETOH compared with controls. The production of IgA and IgG by splenocytes were also significantly decreased by ETOH compared with controls. The levels of IL‐2, IL‐4, and IL‐6 produced by Con A‐stimulated thymocytes were significantly reduced by dietary ETOH compared with control, whereas production of IFN‐γ by thymocytes was not affected. Our results suggest that chronic dietary ETOH alters the cytokine release, thereby impairing immune response and T‐cell maturation, which increase host susceptibility to infection.