Cytokine-activated human endothelial monolayers support enhanced neutrophil transmigration via a mechanism involving both endothelial-leukocyte adhesion molecule-1 and intercellular adhesion molecule-1.

摘要: rIL-1 beta treatment of cultured human endothelial cells (HEC) promotes polymorphonuclear leukocyte (PMN) adhesion and transmigration. Using in vitro quantitative monolayer videomicroscopic transmigration assays, we have examined the contributions endothelial-leukocyte molecule-1 (ELAM-1), intercellular (ICAM-1), complex, CD11/CD18, to these processes. Maximal enhancement PMN were observed after 4 h treatment, when surface expression ELAM-1 had peaked ICAM-1 was modestly increased. Blocking mAb directed either or inhibited greater than 90% up-regulated CD11a/CD18 (LFA-1, a counter-receptor), CD11b/CD18 (Mo-1), CD18 (common 2-integrin) also blocked At later time points (24 48 h), markedly decreased, whereas increased over 4-h level; remained elevated (approximately 50 60% level), but returned levels seen with unactivated HEC. These data indicate that interaction at least two distinct HEC molecules is necessary for transendothelial migration suggests transmigration, although interrelated, are mechanistically