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Am J Physiol Regul Integr Comp Physiol 278: R1140-R1147, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 5, R1140-R1147, May 2000

Role of endotoxin in the expression of endothelial selectins after cecal ligation and perforation

Philippe Bauer1, Cameron W. Lush2, Peter R. Kvietys2, Janice M. Russell1, and D. Neil Granger1

1 Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932; and 2 Department of Physiology, University of Western Ontario and Vascular Biology Program, London Health Sciences Centre, London, Ontario, Canada N6A 4G5

The objectives of this study were to determine 1) the changes in endothelial cell adhesion molecule expression that occur in a clinically relevant model of sepsis and 2) the dependence of these changes on endotoxin [lipopolysaccharide (LPS)]. The dual radiolabeled monoclonal antibody technique was used to quantify the expression of E- and P-selectin in LPS-sensitive (C3HeB/FeJ) and LPS-insensitive (C3H/HeJ) mice that were subjected to acute peritonitis by cecal ligation and perforation (CLP). At 6 h after CLP, the expression of both E- and P-selectin was increased in the gut (mesentery, pancreas, and small and large bowel) compared with the sham-operated and/or control animals, with a more marked response noted in LPS-insensitive mice. The lung also exhibited an increased P-selectin expression in both mouse strains. An accumulation of granulocytes, assessed using tissue myeloperoxidase activity, was noted in the lung and intestine of LPS-sensitive but not LPS-insensitive mice exposed to CLP. These results indicate that the CLP model of sepsis is associated with an upregulation of endothelial selectins in the gut vasculature and that enteric LPS does not contribute to this endothelial cell activation response.

E-selectin; P-selectin; endotoxin-resistant mice; sepsis; shock; myeloperoxidase


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