Chronic ethanol consumption before retrovirus infection is a cofactor in the development of immune dysfunction during murine AIDS.

Abstract

Chronic ethanol (EtOH) consumption has been presumed to be a cofactor in the development of acquired immune deficiency syndrome (AIDS). AIDS is identified as a major public health priority in the United States, with heavy economic and social impact. In the present study, we tested this hypothesis that EtOH users are more predisposed to immunosuppression because of retrovirus infection in murine AIDS. Adult female C57BL/6 mice were fed 4.5% (v/v) in liquid diet and control diets for 10 weeks. Then all mice were infected with LP-BM5 retrovirus, causing murine AIDS, and were fed control liquid diets without EtOH. Interleukin (IL)-2 production produced by concanavalin A (Con A)-stimulated splenocytes was suppressed during murine AIDS. It was further inhibited in EtOH-fed mice compared with controls at 6 weeks postinfection, whereas decreased level of interferon-gamma during murine AIDS was not further affected in EtOH-fed mice. The levels of IL-5, IL-6, and IL-10 secreted by Con A-induced splenocytes, elevated during murine AIDS, were significantly further enhanced in EtOH-fed mice compared with controls at 6 weeks postinfection, whereas retrovirus-induced elevated release of IL-6 and tumor necrosis factor-alpha, produced by lipopolysaccharide (LPS)-stimulated splenocytes, were further increased in EtOH-fed mice compared with controls at 6 and 9 weeks postinfection, respectively. Con A- and LPS-induced splenocyte proliferation, inhibited by retrovirus infection, was significantly further suppressed in EtOH-fed mice compared with controls. These results suggest that dietary EtOH consumption before retrovirus infection aggravated progression of immune dysfunction, because it modified production of immunological regulatory cytokines and immune functions.