Ethanol exacerbates T cell dysfunction after thermal injury

To understand the mechanism of suppressed immunity following alcohol consum ption and thermal injury, we analyzed T cell functions in a mouse model of acute alcohol exposure and burn injury. Mice with blood alcohol levels at a pproximately 100 mg/dl were given a 15% scald or sham injury. Mice were sac rificed 48 h after injury. Our data demonstrated a 20-25% decrease in Con A -mediated splenic T cell proliferation (p < 0.01) and 45-50% decrease in in terleukin-2 (IL-2) production (p < 0.01) following burn injury compared to the T cells from sham animals. A further decrease in the proliferation (25- 30%) and IL-2 production (40-45%) was detected in T cells derived from burn ed animals receiving alcohol as compared to burn alone. No significant chan ge in the proliferation and IL-2 production was observed in splenic T cells derived from sham-injured mice regardless of alcohol exposure. Additionall y, there was no demonstrable difference in splenocyte apoptosis in any trea tment group. These results suggest that alcohol consumption prior to burn i njury causes a greater decrease in T cell proliferation and IL-2 production compared to either burn or alcohol injury alone that may further attenuate the cell-mediated immunity and thus enhance susceptibility to infection. ( C) 2000 Elsevier Science Inc. All rights reserved.