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Alcohol Research Program, Burn and Shock Trauma Institute, Department of Surgery, Loyola University Chicago Medical Center, Maywood, IL 60153
The mechanism of
alcohol-mediated increased infection in burn patients remains unknown.
With the use of a rat model of acute alcohol and burn injury, the
present study ascertained whether acute alcohol exposure before thermal
injury enhances gut bacterial translocation. On day 2 postinjury, we found a severalfold increase in gut bacterial
translocation in rats receiving both alcohol and burn injury compared
with the animals receiving either injury alone. Whereas there were no
demonstrable changes in intestinal morphology in any group of animals,
a significant increase in intestinal permeability was observed in
ethanol- and burn-injured rats compared with 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 interferon-
by gut lymphoid T cells 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+ cell 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 extraintestinal sites.
T lymphocyte; infection immunity bacteria; inflammation; shock
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