Sacks T, Moldow C F, Craddock P R, Bowers T K, Jacob H S
J Clin Invest. 1978 May;61(5):1161-7. doi: 10.1172/JCI109031.
During hemodialysis, alternative pathway complement activation leads to pulmonary sequestration of granulocytes, with loss of pulmonary vascular endothelial integrity and, at times, protein-rich pulmonary edema. An in vitro model of this phenomenon was constructed utilizing 51Cr-labeled human umbilical vein endothelial cell cultures. In this system, granulocytes, when exposed to activated complement (C), induce endothelial damage; this injury is mediated primarily by oxygen radicals produced by the granulocytes. C5a appears to be the C component responsible for granulocyte-induced cytotoxicity; studies with cytochalasin B-treated granulocytes suggest that close approximation of the granulocytes and endothelial cells is necessary for maximal cell injury.
在血液透析过程中,替代途径补体激活导致粒细胞在肺部潴留,肺血管内皮完整性丧失,有时还会出现富含蛋白质的肺水肿。利用51Cr标记的人脐静脉内皮细胞培养构建了这一现象的体外模型。在该系统中,粒细胞在接触活化补体(C)时会诱导内皮损伤;这种损伤主要由粒细胞产生的氧自由基介导。C5a似乎是负责粒细胞诱导的细胞毒性的补体成分;用细胞松弛素B处理粒细胞的研究表明,粒细胞与内皮细胞的紧密接近对于最大程度的细胞损伤是必要的。