Mechanisms of suppression of cellular immunity induced by ethanol

Abstract

Previous study findings from this laboratory and other laboratories have established that ethanol administration to experimental animals or ingestion by human beings results in many changes in the immune system. The major effort in this laboratory is the study of the mechanisms by which ethanol down-regulates the responses of thymus-derived lymphocytes. By using a rat model of ethanol intoxication we have described a defect in lymphocyte proliferation to concanavalin A. In the current report data, preliminary and definitive, are presented that show our approach to determining the mechanisms of ethanol-associated impairments in the immune system, especially the defect in lymphocyte proliferation. We have found that purified thymus-derived lymphocytes from the spleens of ethanol-treated rats have an inherent defect in their response to mitogenic stimulation. This defect is not caused by the direct effects of ethanol on the cells and probably is not caused by an inability of the cells from ethanol-treated animals to produce the lymphocyte growth factor interleukin 2. Data are also presented that indicate that corticosteroids, produced most abundantly in this model by withdrawal from ethanol, play a role in the down-regulation of the response of spleen cells to mitogenic stimulation.