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Ethanol exacerbates T cell dysfunction after thermal injury
Journal article   Peer reviewed

Ethanol exacerbates T cell dysfunction after thermal injury

Mashkoor A Choudhry, Kelly A.N Messingham, Shahla Namak, Alessandra Colantoni, Christine V Fontanilla, Lisa A Duffner, Mohammed M Sayeed and Elizabeth J Kovacs
Alcohol (Fayetteville, N.Y.), Vol.21(3), pp.239-243
2000
DOI: 10.1016/S0741-8329(00)00093-8
PMID: 11091027

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Abstract

To understand the mechanism of suppressed immunity following alcohol consumption 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 approximately 100 mg/dl were given a 15% scald or sham injury. Mice were sacrificed 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 interleukin-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 burned animals receiving alcohol as compared to burn alone. No significant change in the proliferation and IL-2 production was observed in splenic T cells derived from sham-injured mice regardless of alcohol exposure. Additionally, there was no demonstrable difference in splenocyte apoptosis in any treatment group. These results suggest that alcohol consumption prior to burn injury 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.
Mice Interleukin-2 T cell proliferation Splenocytes Burn injury Apoptosis

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