Role of endotoxin in intestinal reperfusion-induced expression of E-selectin

Products of enteric bacteria, including endotoxin [Lipopolysaccharide (LPS) ], have been implicated in the acute inflammatory responses elicited by isc hemia and reperfusion (I/R) of the small intestine. The objective of this s tudy was to assess the contribution of LPS to the increased E-selectin expr ession observed in the intestinal vasculature after I/R. The dual radiolabe led monoclonal antibody technique was used in LPS-sensitive (C3HeB/FeJ) and LPS-insensitive (C3H/HeJ) mice that were exposed to either exogenous LPS o r to gut YR (45 min ischemia, 5 h reperfusion). LPS elicited a dose-depende nt (0.5-50 mu g LPS/animal) increase in E-selectin expression (at 3 h) in L PS-sensitive mice, whereas LPS-insensitive mice were largely unresponsive. E-selectin expression was increased fivefold by I/R in the small bowel of b oth LPS-sensitive and -insensitive mice. These results indicate that, altho ugh 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.