Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage

T. Sacks, C. F. Moldow, P. R. Craddock, T. K. Bowers, Harry S Jacob

Research output: Contribution to journalArticlepeer-review

787 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1161-1167
Number of pages7
JournalUnknown Journal
Volume61
Issue number5
DOIs
StatePublished - 1978

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