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• W2146800979 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." @default.
• W2146800979 created "2016-06-24" @default.
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• W2146800979 date "1978-05-01" @default.
• W2146800979 modified "2023-09-26" @default.
• W2146800979 title "Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage." @default.
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• W2146800979 doi "https://doi.org/10.1172/jci109031" @default.
• W2146800979 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/372636" @default.
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