Ethanol exacerbates T cell dysfunction after thermal injury

Choudhry, Mashkoor A; Messingham, Kelly A.N; Namak, Shahla; Colantoni, Alessandra; Fontanilla, Christine V; Duffner, Lisa A; Sayeed, Mohammed M; Kovacs, Elizabeth J

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Volume 21, Issue 3 , Pages 239-243, July 2000

Ethanol exacerbates T cell dysfunction after thermal injury

Mashkoor A Choudhry
- Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Surgery, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Corresponding author. Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA. Tel.: +1-708-327-2451; fax: +1-708-327-2813
Kelly A.N Messingham
- Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Shahla Namak
- Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Alessandra Colantoni
- Department of Medicine, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Christine V Fontanilla
- Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Lisa A Duffner
- Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Mohammed M Sayeed
- Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Surgery, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Physiology, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Elizabeth J Kovacs
- Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Surgery, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
- Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA

Received 13 January 2000; received in revised form 23 March 2000; accepted 30 March 2000.

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.

Keywords: Apoptosis, Burn injury, Interleukin-2, Mice, Splenocytes, T cell proliferation