Abstract
Tumor necrosis factor-alpha (TNF-alpha), a product of monocytes and macrophages, functions as an important proinflammatory cytokine in the host's response to invading pathogens. Because both alcohol abuse and human immunodeficiency virus infection affect TNF-alpha production and are known to frequently coexist, this study examined the effects of simian immunodeficiency virus (SIV) infection and in vitro alcohol exposure on the lipopolysaccharide (LPS)-induced TNF-alpha response in blood obtained from SIV-negative and -positive animals at the asymptomatic and terminal stages of infection. Spontaneous TNF-alpha production was undetectable or low in all groups examined. LPS-induced TNF-alpha production was increased in blood obtained at the asymptomatic (746 +/- 226 pg/ml) and terminal (1945 +/- 1013 pg/ml) stages, compared with that from SIV-negative animals (210 +/- 28 pg/ml), whereas TNF-alpha messenger RNA content did not differ in LPS-stimulated blood obtained from SIV-negative, asymptomatic SIV-positive, or terminal SIV-positive animals. Ethanol treatment suppressed TNF-alpha protein production in all groups, whereas TNF-alpha messenger RNA levels remained unchanged in blood obtained from animals not infected with SIV. Blood cellular elements remain responsive to LPS stimulation with respect to TNF production even into the acquired immunodeficiency syndrome stage of SIV disease. However, intoxicating doses of alcohol suppress this response, and this may contribute to the immunocompromised state of the host.
Published Version
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