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Am J Physiol Gastrointest Liver Physiol 280: G291-G297, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 2, G291-G297, February 2001

Endothelial E- and P-selectin expression in iNOS- deficient mice exposed to polymicrobial sepsis

Cameron W. Lush, Gediminas Cepinskas, William J. Sibbald, and Peter R. Kvietys

Department of Physiology, University of Western Ontario, London, N6A 5C1; and Vascular Biology Program, Lawson Health Research Institute, London, Ontario, Canada, N6A 4G5

In vitro, nitric oxide (NO) decreases leukocyte adhesion to endothelium by attenuating endothelial adhesion molecule expression. In vivo, lipopolysaccharide-induced leukocyte rolling and adhesion was greater in inducible NO synthase (iNOS)-/- mice than in wild-type mice. The objective of this study was to assess E- and P-selectin expression in the microvasculature of iNOS-/- and wild-type mice subjected to acute peritonitis by cecal ligation and perforation (CLP). E- and P-selectin expression were increased in various organs within the peritoneum of wild-type animals after CLP. This CLP-induced upregulation of E- and P-selectin was substantially reduced in iNOS-/- mice. Tissue myeloperoxidase (MPO) activity was increased to a greater extent in the gut of wild-type than in iNOS-/- mice subjected to CLP. In the lung, the reduced expression of E-selectin in iNOS-/- mice was not associated with a decrease in MPO. Our findings indicate that NO derived from iNOS plays an important role in sepsis-induced increase in selectin expression in the systemic and pulmonary circulation. However, in iNOS-/- mice, sepsis-induced leukocyte accumulation is affected in the gut but not in the lungs.

neutrophils; cecal ligation and perforation; myeloperoxidase activity; intracellular adhesion molecule-2


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