Boogaerts M A, Yamada O, Jacob H S, Moldow C F
Proc Natl Acad Sci U S A. 1982 Nov;79(22):7019-23. doi: 10.1073/pnas.79.22.7019.
Complement-stimulated granulocytes adhere to and induce significant 51Cr release from endothelial cells in vitro. Platelets were stimulated to undergo release, and these release products significantly enhanced granulocyte-endothelial cell adherence and granulocyte-induced 51Cr release from endothelial cells. Platelet serotonin appeared to mediate these phenomena because serotonin antagonists blocked both the enhanced endothelial adherence and 51Cr release. In addition, added serotonin mimicked the effect seen with the stimulated platelets upon granulocyte--endothelial cell adherence and cytotoxicity completely. This enhancement appeared to be due to serotonin effects upon both the granulocyte and endothelial cells. These data suggest that a released platelet constituent might modulate in vivo granulocyte-endothelial cell interactions in clinical disorders.
补体刺激的粒细胞在体外可黏附于内皮细胞并诱导其释放大量的51Cr。血小板被刺激后发生释放,这些释放产物显著增强了粒细胞与内皮细胞的黏附以及粒细胞诱导的内皮细胞51Cr释放。血小板5-羟色胺似乎介导了这些现象,因为5-羟色胺拮抗剂可阻断增强的内皮细胞黏附及51Cr释放。此外,添加的5-羟色胺完全模拟了刺激血小板对粒细胞与内皮细胞黏附及细胞毒性的影响。这种增强似乎是由于5-羟色胺对粒细胞和内皮细胞均有作用。这些数据表明,在临床疾病中,血小板释放的一种成分可能会调节体内粒细胞与内皮细胞的相互作用。