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A possible mechanism for vascular endothelial cell injury elicited by activated leukocytes: a significant involvement of adhesion molecules, CD11/CD18, and ICAM-1.

To clarify the mechanism of vascular endothelial cell injury induced by activated leukocytes, we investigated the intracellular peroxide level in endothelial cells and the effect of antibodies against adhesion molecules on it. The change in the intracellular peroxide level was measured using the fluorescence of 2,7-dichlorofluorescein diacetate. The fluorescence intensity of the endothelial cells exposed to PMA-stimulated leukocytes increased with time up to 15 min, although neither PMA alone nor unstimulated leukocytes alone showed such increase at all. When catalase, which degrades hydrogen peroxide produced by leukocytes, was added to this system, the peroxide level in endothelial cells decreased significantly. On the other hand, pretreatment of endothelial cells with allopurinol, a specific inhibitor of xanthine oxidase, also caused significant inhibition of the increase in peroxide level in the endothelial cells. The monoclonal antibodies against CD11a, CD11b, CD18, and ICAM-1 showed almost complete inhibition of the increase in intracellular peroxide levels of the endothelial cells exposed to PMA-stimulated leukocytes. In contrast, the anti-CD11c antibody could not block the increase in fluorescence intensity due to peroxides. The endothelial injury elicited by activated leukocytes was partially inhibited by catalase alone (approximately 40%) and allopurinol alone (approximately 60%), but it was completely inhibited by the concomitant treatment of endothelial cells with catalase and allopurinol. The specific antibodies against such adhesion molecules as ICAM-1 and CD11/CD18 except CD11c/CD18 also blocked the endothelial cell injury significantly. These data suggest that there is a good correlation between the early increase in intracellular peroxides and endothelial cell injury elicited by PMA-stimulated leukocytes and that the adhesion of activated leukocytes to endothelial cells via CD11a/CD18-ICAM-1 must be deeply involved in these phenomena.