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Am J Physiol Gastrointest Liver Physiol (January 23, 2002). doi:10.1152/ajpgi.00235.2001
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Articles in PresS, published online ahead of print January 23, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00235.2001
Submitted on June 8, 2001
Accepted on January 18, 2002

Gut-Associated Lymphoid T Cell Suppression Enhances Bacterial Translocation in Alcohol and Burn Injury

Mashkoor A Choudhry1*, Nadeem Fazal1, Masakatsu Goto2, Richard L Gamelli1, and Mohammed M Sayeed1

1 Alcohol Research Program, Loyola University Medical Center, Maywood, IL, USA; Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL, USA; Department of Surgery, Loyola University Medical Center, Maywood, IL, USA
2 ; Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, IL, USA; Department of Surgery, Loyola University Medical Center, Maywood, IL, USA

* To whom correspondence should be addressed. E-mail: mchoudh{at}lumc.edu.

The mechanism of alcohol-mediated increased infection in burn patients remains unknown. Utilizing a rat model of acute alcohol and burn injury, the present study ascertained if acute alcohol exposure prior to thermal injury enhances gut bacterial translocation. On day 2 post injury, we found a several fold increase in gut bacterial translocation in rats receiving both alcohol and burn injury compared to the animals receiving either injury alone. While there were no demonstrable changes in intestinal morphology in any group of animals, a significant increase in intestinal permeability was observed in Etoh and burn injured rats compared to the rats receiving either injury alone. We further examined the role of intestinal immune defense by determining the gut associated lymphoid (Peyer's patches and mesenteric lymph nodes) T cell effector responses 2 days after alcohol and burn injury. Although there was a decrease in the proliferation and IFN-{gamma} by gut lymphoid T cell after burn injury alone; the suppression was maximum in the group of rats receiving both alcohol and burn injuries. Furthermore, the depletion of CD3+ cells in healthy rats resulted in bacterial accumulation in mesenteric lymph nodes; such CD3+ cells depletion in alcohol and burn injured rats furthered the spread of bacteria to spleen and circulation. In conclusion, our data suggest that the increased intestinal permeability and a suppression of intestinal immune defense in rats receiving alcohol and burn injury may cause an increase in bacterial translocation and their spread to extra-intestinal sites.




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