Alcoholics are known to be very susceptible to infections. We studied the effects of alcohol on the immune system of rats and mice using various models to produce physical dependence. Both normal and adrenalectomized animals were studied with respect with respect to cell numbers and cell function. Ethanol administration resulted in the loss of lymphocytes from the peripheral blood, spleen and thymus regardless of the route of ethanol administration (intubation or inhalation in rats, liquid diet for mice). Intubation and liquid diet resulted in a decrease in the ability of lymphocytes from the spleen and peripheral blood to respond to nonspecific mitogens while no such decrease in proliferative ability was noted in rats administered ethanol by inhalation. Adrenalectomy reversed the decrease in ability of lymphocytes to respond to mitogens. The ability to mount a primary immune response was tested using SRBC and TNP-ficol immunization. Animals treated with ethanol showed a decreased ability to respond to the T-cell dependent antigen SRBC but no change in their ability to respond to the T-cell independent antigen TNP-ficol when compared to controls. The ability to mount a primary immune response to SRBC was not reversed by adrenalectomy. IL2 production was monitored during ethanol administration and was found to be increased in comparison to control at the same time that proliferation was decreased. IL2 receptor numbers also appear to be increased in ethanol treated animals. Studies were performed to examine the link between the immune and central nervous systems using IL2 binding to brain tissue as a model.
