ETHANOL-INDUCED MODULATION OF CYTOKINE PRODUCTION BY SPLENOCYTES DURING MURINE RETROVIRUS INFECTION CAUSING MURINE AIDS

Ethanol (ETOH) consumption has been associated with general suppressio n of the immune response, resulting in increased susceptibility to inf ection. Chronic dietary ETOH consumption may be one of the cofactors a ccelerating development of human acquired immune deficiency syndrome ( AIDS) after retrovirus infection. Chronic dietary ETOH [5% (v/v)] in t he Lieber-DeCarli liquid diet was fed female C57BL/6 mice inoculated w ith LP-BM5 retrovirus causing murine AIDS for 11 weeks. Because cytoki nes are key regulators of humoral and cellular immunity, their product ion by concanavalin A (ConA) and lipopolysaccharide (LPS)-induced sple nocytes was measured by ELISA methods. Decreased levels of interleukin (IL)-2 caused by retrovirus infection remained unchanged. Elevated le vels of IL-5 and IL-6 produced in vitro by ConA-stimulated spleen cell s during retrovirus infection were significantly further increased by dietary ETOH. Elevated IL-4 due to retroviral infection were not affec ted by dietary ETOH. Increased production of IL-10 induced by retrovir us infection, however, was significantly reduced by dietary ETOH, wher eas decreased release of interferon-T induced by retrovirus infection was significantly enhanced. Elevated levels of tumor necrosis factor-a lpha produced by LPS-stimulated splenocytes from retrovirus infected m ice were significantly further increased by dietary ETOH, whereas leve ls of IL-6 by LPS-stimulated splenocytes were not affected. Suppressed T-cell proliferation caused by retrovirus infection was significantly reduced further by dietary ETOH. However, no effect of dietary ETOH w as observed on decreased B-cell proliferation by retrovirus infection. These results suggest that dietary ETOH aggravates progression of imm une dysfunction leading to AIDS, because dietary ETOH modifies product ion of immunological regulatory cytokines.