Ethanol enhances activation-induced caspase-3 dependent cell death in T lymphocytes
Abstract
Clinical and experimental studies have shown that an important deleterious consequence of excessive alcohol consumption is immunosuppression, specifically, a depletion in the mature CD4+ T-cell population. A predominant mechanism involved in T-cell depletion is activation-induced cell death (AICD). Although it is well documented that ethanol intake can cause depletion of CD4+ T cells, the mechanism of how alcohol mediates its effects is unclear. The results were based on data from three separate experiments presented as mean +/- standard deviation (SD). Jurkat CD4+ T cells and peripheral blood lymphocytes were treated with 25 mM of ethanol (12-18 hr), followed by stimulation with mitogens Conconavalin A (5 microg/ml) and Phytohemmaglutinin (1 microg/ml) or T-cell receptor ligation (anti-CD3 antibody (5 microg/ml)) for 6 hr, and then harvested for measurement. The apoptotic cell death markers measured include cell viability, Caspase-3-like activity, and DNA fragmentation. We demonstrate that alcohol pretreatment enhances AICD of Jurkat CD4+ T cells and peripheral blood lymphocytes upon activation by CD3-crosslinking or stimulation with Conconavalin A and Phytohemmaglutinin. Furthermore, we find that the ethanol-mediated enhancem...Continue Reading
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