Ethanol-induced modulation of cytokine production by splenocytes during murine retrovirus infection causing murine AIDS.
Ethanol (ETOH) consumption has been associated with general suppression of the immune response, resulting in increased susceptibility to infection. Chronic dietary ETOH consumption may be one of the cofactors accelerating development of human acquired immune deficiency syndrome (AIDS) after retrovirus infection. Chronic dietary ETOH [5% (v/v)] in the Lieber-DeCarli liquid diet was fed female C57BL/6 mice inoculated with LP-BM5 retrovirus causing murine AIDS for 11 weeks. Because cytokines are key regulators of humoral and cellular immunity, their production by concanavalin A (ConA) and lipopolysaccharide (LPS)-induced splenocytes was measured by ELISA methods. Decreased levels of interleukin (IL)-2 caused by retrovirus infection remained unchanged. Elevated levels of IL-5 and IL-6 produced in vitro by ConA-stimulated spleen cells during retrovirus infection were significantly further increased by dietary ETOH. Elevated IL-4 due to retroviral infection were not affected by dietary ETOH. Increased production of IL-10 induced by retrovirus infection, however, was significantly reduced by dietary ETOH, whereas decreased release of interferon-tau induced by retrovirus infection was significantly enhanced. Elevated levels of tumor necrosis factor-alpha produced by LPS-stimulated splenocytes from retrovirus infected mice were significantly further increased by dietary ETOH, whereas levels 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 was observed on decreased B-cell proliferation by retrovirus infection. These results suggest that dietary ETOH aggravates progression of immune dysfunction leading to AIDS, because dietary ETOH modifies production of immunological regulatory cytokines.
Wang
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Y
Department of Family and Community Medicine, University of Arizona, Tucson 85724.
Huang
D S
DS
Giger
P T
PT
Watson
R R
RR
D000428:Alcohol Drinking / Q000009:adverse effects* / Q000276:immunology; D000437:Alcoholism / Q000276:immunology*; D000818:Animals; D001402:B-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007108:Immune Tolerance / Q000187:drug effects / Q000502:physiology; D007371:Interferon-gamma / Q000096:biosynthesis; D007378:Interleukins / Q000096:biosynthesis; D051379:Mice; D008810:Mice, Inbred C57BL; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D016207:Cytokines; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma