Nitric Oxide Modulates Leukocyte—Endothelial Cell Adhesion

Abstract

Although the role of leukocytes in certain inflammatory diseases (e.g., arthritis, inflammatory bowel diseases) has long been appreciated, there is a large body of recent evidence that implicates leukocytes in a number of other pathological conditions, including atherosclerosis, hypertension, ischemia—reperfusion injury, venous thrombosis, and gastric ulceration. The recognition that a leukocyte must first adhere to vascular endothelium before it can exert its deleterious effects on blood vessels and neighboring parenchymal cells has led to an intensive effort to define the factors that influence the ability of leukocytes to adhere to endothelial cells. Data derived from both in vitro and in vivo models of leukocyte—endothelial cell adhesion invoke a role for several factors in the modulation of this cell-adhesion process. These factors include adhesion glycoproteins that are expressed on the surface of activated leukocytes and endothelial cells, hydrodynamic dispersal forces (e.g., shear rate) that are generated by the movement of blood through the circulation, and some products of leukocyte and endothelial cell activation.