| First Author | Chosay JG | Year | 1998 |
| Journal | Am J Physiol | Volume | 274 |
| Issue | 4 Pt 1 | Pages | G776-82 |
| PubMed ID | 9575861 | Mgi Jnum | J:47143 |
| Mgi Id | MGI:1202661 | Doi | 10.1152/ajpgi.1998.274.4.G776 |
| Citation | Chosay JG, et al. (1998) Role of PECAM-1 (CD31) in neutrophil transmigration in murine models of liver and peritoneal inflammation. Am J Physiol 274(4 Pt 1):G776-82 |
| abstractText | Platelet endothelial cell adhesion molecule-1 (PECAM-1) is thought to be critical for transendothelial migration of leukocytes, including neutrophils. Because neutrophil-mediated liver injury during endotoxemia is dependent on transmigration, we investigated the role of PECAM-1 in the pathophysiology of endotoxin-induced liver injury. Male C3Heb/FeJ mice were treated with galactosamine (Gal) and endotoxin (ET) (700 mg/kg Gal/100 micrograms/kg ET), and liver sections were stained for PECAM-1 expression. Control livers showed the presence of PECAM-1 on endo-thelial cells of large vessels but not in sinusoids. Gal/ET treatment did not change the expression pattern of PECAM-1. Gal/ET-induced liver injury (area of necrosis: 38 +/- 3%) was not attenuated by treatment with 3 mg/kg of the antimurine PECAM-1 antibody 2H8. The antibody had no effect on sequestration and transmigration of neutrophils in sinusoids or the margination of neutrophils in large vessels. In contrast, 2H8 inhibited glycogen-induced neutrophil migration into the peritoneum by 74%; this effect correlated with PECAM- 1 expression in the intestinal vasculature. Thus PECAM-1 is neither expressed nor inducible in hepatic sinusoids and is consequently not involved in neutrophil transmigration in the liver during endotoxemia. On the other hand, expression of PECAM-1 in mesenteric veins is critical for peritoneal neutrophil accumulation. |
