Immune dysfunction during alcohol consumption and murine AIDS: The protective role of dehydroepiandrosterone sulfate

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by the human immunodeficiency virus (HIV) after development of severe immunos uppressive changes. Chronic ethanol (EtOH) consumption accentuates the seve rity of murine AIDS (MAIDS). Because hormone production is often suppressed by chronic EtOH intake, as well as retrovirus infection, we investigated w hether hormone supplementation during chronic EtOH consumption contributes to slowing immune dysfunction caused by LP-BM5 infection and/or EtOH use. B ecause dehydroepiandrosterone sulfate (DHEAS) was previously shown to have immune-enhancing properties during MAIDS, we determined whether DHEAS reduc ed cytokine dysregulation otherwise exacerbated by chronic EtOH intake duri ng MAIDS. Adult female C57BL/6 mice were infected with LP-BM5 murine retrov irus. Some were fed 40% EtOH in drinking water and agar gel for 16 weeks po stinfection. EtOH consumption further inhibited T- and B-cell proliferation beyond suppression due to retrovirus infection. Interleukin (IL)-2 release produced by concanavalin A-stimulated splenocytes was reduced by EtOH use by infected and uninfected mice. DHEAS overcame much of the effects induced by retrovirus infection and/or EtOH use. IL-4 secretion and IL-6 secretion were enhanced. Hepatic vitamin E levels were decreased by murine retroviru s infection, as well as by EtOH use in both uninfected and infected mice. I n addition, DHEAS (0.01%) supplementation during MAIDS prevented the furthe r dysregulation of cytokines and hepatic lipid peroxidation due to EtOH int ake, partially restored T- and B-cell proliferation, and maintained hepatic vitamin E levels to near normal levels.