ABSTRACT
The adhesion of leukocytes to vascular endothelium is a hallmark of the inflammatory process. The requirement for and participation of specific adhesion glycoproteins in the binding of leukocytes to endothelial cells has been elegantly demonstrated using a variety of experimental approaches (1,2). However, our current understanding of the molecular basis for leukocyte-endothelial cell adhesion is largely based on data generated from studies utilizing isolated leukocytes and monolayers of cultured endothelial cells. Much of this information was derived from relatively few endothelial cell models, most notably human umbilical cord endothelial cells (HUVEC). The importance of the HUVEC monolayer model to the field of inflammation research cannot be overstated (1,2). It led to the discovery and characterization of a number of key cell adhesion molecules (CAMs) expressed on endothelial cells and/or leukocytes that are now known to mediate adhesive interactions such as leukocyte rolling, firm adhesion, and emigration. This in vitro model has also provided quantitative insights into the modulating role of physical factors such as shear stress on leukocyte-endothelial cell adhesion. Similarities in the time-course and magnitude of CAM expression following activation of different endothelial cell populations grown in culture have led to the general perception that endothelial cells distributed throughout the body are relatively homogeneous in their responses and contributions to inflammatory stimuli.
