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Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130-3932
Products of
enteric bacteria, including endotoxin [lipopolysaccharide
(LPS)], have been implicated in the acute inflammatory responses
elicited by ischemia and reperfusion (I/R) of the small intestine. The objective of this study was to assess the contribution of LPS to the increased E-selectin expression observed in the intestinal vasculature after I/R. The dual radiolabeled monoclonal antibody technique was used in LPS-sensitive (C3HeB/FeJ) and
LPS-insensitive (C3H/HeJ) mice that were exposed to either exogenous
LPS or to gut I/R (45 min ischemia, 5 h reperfusion). LPS
elicited a dose-dependent (0.5-50 µg LPS/animal) increase in
E-selectin expression (at 3 h) in LPS-sensitive mice, whereas
LPS-insensitive mice were largely unresponsive. E-selectin expression
was increased fivefold by I/R in the small bowel of both LPS-sensitive
and -insensitive mice. These results indicate that, although exogenous
LPS is capable of eliciting profound dose-dependent increases in
E-selectin expression, endogenous LPS does not contribute significantly
to I/R-induced expression of this endothelial cell adhesion molecule.
lipopolysaccharide; endotoxin-resistant mice; enteric bacteria; tumor necrosis factor-
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