| First Author | Lush CW | Year | 2001 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 280 |
| Issue | 2 | Pages | G291-7 |
| PubMed ID | 11208553 | Mgi Jnum | J:68060 |
| Mgi Id | MGI:1931992 | Doi | 10.1152/ajpgi.2001.280.2.G291 |
| Citation | Lush CW, et al. (2001) Endothelial E- and P-selectin expression in iNOS- deficient mice exposed to polymicrobial sepsis. Am J Physiol Gastrointest Liver Physiol 280(2):G291-7 |
| abstractText | 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. |
