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.
|Original language||English (US)|
|Number of pages||5|
|Journal||American Journal of Pathology|
|State||Published - 1981|