Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.
作者： T Sacks , C F Moldow , P R Craddock , T K Bowers , H S Jacob
DOI: 10.1172/JCI109031
关键词:
摘要: During hemodialysis, alternative pathway complement activation leads to pulmonary sequestration of granulocytes, with loss vascular endothelial integrity and, at times, protein-rich edema. An in vitro model this phenomenon was constructed utilizing 51Cr-labeled human umbilical vein cell cultures. In system, when exposed activated (C), induce damage; injury is mediated primarily by oxygen radicals produced the granulocytes. C5a appears be C component responsible for granulocyte-induced cytotoxicity; studies cytochalasin B-treated granulocytes suggest that close approximation and cells necessary maximal injury.
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