Endothelial-leukocyte adhesive interactions in inflammatory diseases.

There is evidence that vascular endothelium directs the accumulation of leukocytes in inflammation through various means, particularly by the expression of specific cell surface molecules which are adhesive for ligands on circulating leukocytes. Examples of such molecules are E-selectin and intercellular adhesion molecule 1 (ICAM-1). In an experimental model of various forms of inflammation, E-selectin and ICAM-I were induced in association with adhesion and emigration of circulating polymorphonuclear and mononuclear leukocytes. Further work in humans showed endothelium to express E-selectin in inflammation. In addition, the presence of a leukocyte ligand for E-selectin, sialyl-Lewis X, has been seen on cells accumulating in inflammation. Furthermore, sialyl-Lewis X was also unexpectedly seen on endothelium. The role of sialyl-Lewis X on endothelium is as yet uncertain, although it may function as an adhesion receptor for leukocytes. Other endothelial adhesion receptors, such as vascular cell adhesion molecule 1 (VCAM-1), are described. Atherosclerosis shows many features in common with inflammation. These are discussed, and the demonstrated and potential relevance of endothelial adhesive phenomena in routine inflammation to those in atherosclerosis are reviewed. For example, a VCAM-1 homologue has been described on the endothelium over evolving atherosclerotic lesions in rabbits.