Abstract

There is controversy concerning whether intravascular activation of neutrophils during acute inflammation injuries contiguous endothelial cells in vivo. Several physiologic defense mechanisms tend to limit such injury. In this paper we have examined evidence for one of these putative protective mechanisms: endothelial cell modulation of the activation responses of neutrophils during adherence and diapedesis. In vitro, endothelial cells co-incubated with neutrophils inhibit the release of superoxide anion when stimulated by receptor-mediated activators. The possible mechanisms include contact-linked down-regulation of neutrophil activation, the release from endothelial cells of soluble mediators which attenuate neutrophil activation responses, and the presence of free radical scavengers in endothelial cells which are active at the interface between endothelial cells and adherent neutrophils. There may be a broad spectrum of mechanisms by which intercellular interactions protect the lining cells of the vascular lumen from 'inadvertent' destruction by phagocytes which become activated while in an intravascular location.