title: Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.
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.
mesh_terms: D001808:Blood Vessels / Q000473:pathology*; D002478:Cells, Cultured; D003165:Complement System Proteins / Q000378:metabolism*; D004727:Endothelium / Q000473:pathology; D005609:Free Radicals; D006098:Granulocytes / Q000502:physiology*; D006801:Humans; D007962:Leukocytes / Q000502:physiology*; D008247:Lysosomes / Q000201:enzymology; D009504:Neutrophils / Q000502:physiology; D010100:Oxygen; D009195:Peroxidase / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects; D013481:Superoxides
chemical_list: D005609:Free Radicals; D013481:Superoxides; D003165:Complement System Proteins; D009195:Peroxidase; D010100:Oxygen