VE-CADHERIN ANTIBODY ACCELERATES NEUTROPHIL RECRUITMENT IN-VIVO

Neutrophils enter sites of inflammation by crossing the endothelial li ning of the blood vessel wall. VE-cadherin is an endothelial specific, hemophilic adhesion molecule located at the lateral cell surface. We have generated a monoclonal antibody against mouse VE-cadherin which i nhibits electrical resistance of endothelial cell monolayers in vitro as well as aggregation of VE-cadherin transfected cells. In vivo, this antibody was found to increase vascular permeability and to accelerat e the entry of neutrophils into chemically inflamed mouse peritoneum. Thus, VE-cadherin is essential for the integrity of the endothelial ba rrier in vivo. Our data suggest that opening of VE-cadherin mediated e ndothelial cell contacts may be a relevant step during neutrophil extr avasation.