ABSTRACT
Expression of intercellular adhesion molecule 1 (ICAM-1) and vascular adhesion molecule 1 (VCAM-1) on endothelial cells causes extravasation of T cells and
monocytes/macrophages into tissue sites. Th e expression of ligands for these molecules (Tables 1, 2) (Rahman and Fazal 2009) helps to determine sites of adhesion followed by extravasation. Th e choice of a paracellular versus transcellular leukocyte migration pathway depends upon the tightness of the intercellular junctions of the endothelial cells, the type of stimuli, the type of leukocytes and the endothelial cell source. Rahman and Fazal note that transcellular leukocyte migration appears to occur more prominently in vascular areas where endothelial junctions are particularly tight, such as the blood-brain barrier, while paracellular migration of leukocytes occurs in vascular areas in which the endothelial junctions are less tight, such as postcapillary venules. Activation of endothelium may result from release of infl ammatory cytokines (IL-1, TNF-α, IL-6) by endothelial cells and/or monocytes/macrophages following endothelial injury during reperfusion or by the gas bubbles causing DCS (Table 3). In the development of DCS, the surface of nitrogen bubbles that appear in the blood, extracellular space, and intracellular space during decompression may trigger an infl ammation and activation of a cytokine cascade (Ersson et al. 1998, 2002) that increases ICAM-1/ VCAM-1 expression. Key Points Endothelium is activated by infl ammatory molecules called cytokines. Blood leukocytes expressing certain CAMs interact with endothelial co-ligands, which permits transmigration of blood leukocytes into the injured tissue site.
