title: Complement-induced granulocyte aggregation in vivo.
abstract: Previous studies from our laboratories have demonstrated that granulocytes (PMNs), when exposed to activated complement (C) (specifically C5a), will aggregate and be provoked to damage cultured endothelial cells in vitro; it was postulated that these phenomena might also occur in vivo, constituting a previously unsuspected mechanism of immune tissue damage. The studies here presented confirm by intravital microscopy that PMN aggregation and leukoembolization in fact occur in live animals when C is activated or C5a is infused, and that these are accompanied by extravasation of plasma proteins in a pattern suggesting endothelial damage. It is concluded that altered microvascular behavior of PMNs is a possible pathogenetic mechanism in disease states associated with C activation.
mesh_terms: D000818:Animals; D001011:Aorta; D001160:Arterioles / Q000187:drug effects / Q000473:pathology; D002449:Cell Aggregation; D003167:Complement Activation; D003165:Complement System Proteins / Q000276:immunology*; D004617:Embolism / Q000209:etiology / Q000276:immunology; D004727:Endothelium / Q000473:pathology; D005260:Female; D006098:Granulocytes / Q000276:immunology*; D008775:Methylprednisolone / Q000494:pharmacology; D008856:Microscopy, Fluorescence / Q000379:methods; D009504:Neutrophils / Q000276:immunology; D051381:Rats; D014743:Videotape Recording
chemical_list: D003165:Complement System Proteins; D008775:Methylprednisolone