Gimbrone M A, Brock A F, Schafer A I
J Clin Invest. 1984 Oct;74(4):1552-5. doi: 10.1172/JCI111570.
Adhesion of polymorphonuclear leukocytes (PMN) to the endothelial lining of blood vessels is an essential component of the inflammatory response. We have examined the effects of various lipoxygenase metabolites of arachidonic acid on PMN adhesion to cultured vascular endothelial cells, using a quantitative monolayer adhesion assay. Our results indicated that leukotriene B4 (LTB4) could effectively stimulate PMN adhesion to endothelial cell surfaces, in contrast to the sulfidopeptide leukotrienes C4, D4, and E4, and the monohydroxyacid lipoxygenase products of leukocytes and platelets, 5S-hydroxy-6-trans-8,11,14-cis-eicosatetraenoic acid and 12S-hydroxy-5,8-cis,10-trans,14-cis-eicosatetraenoic acid, respectively. LTB4-stimulation of PMN-endothelial adhesion did not appear to be dependent upon the generation of cyclooxygenase metabolites, nor was it inhibited by exogenous prostacyclin. Enhanced PMN adhesion was observed with endothelial cells that were cultured from different types of large vessels (arteries and veins) in several species. These findings suggest an important pathophysiologic role for LTB4 in regulating leukocyte-vessel wall interactions.
多形核白细胞(PMN)与血管内皮的黏附是炎症反应的重要组成部分。我们使用定量单层黏附试验,研究了花生四烯酸的各种脂氧合酶代谢产物对PMN与培养的血管内皮细胞黏附的影响。我们的结果表明,与硫肽白三烯C4、D4和E4以及白细胞和血小板的单羟基酸脂氧合酶产物(分别为5S-羟基-6-反式-8,11,14-顺式-二十碳四烯酸和12S-羟基-5,8-顺式,10-反式,14-顺式-二十碳四烯酸)相比,白三烯B4(LTB4)能有效刺激PMN与内皮细胞表面的黏附。LTB4对PMN-内皮黏附的刺激似乎不依赖于环氧化酶代谢产物的生成,也不受外源性前列环素的抑制。在几种物种中,从不同类型的大血管(动脉和静脉)培养的内皮细胞中均观察到PMN黏附增强。这些发现提示LTB4在调节白细胞-血管壁相互作用中具有重要的病理生理作用。