Complement-induced granulocyte aggregation in vivo

Am J Pathol. 1981 Feb;102(2):146-50.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Aorta
  • Arterioles / drug effects
  • Arterioles / pathology
  • Cell Aggregation
  • Complement Activation
  • Complement System Proteins / immunology*
  • Embolism / etiology
  • Embolism / immunology
  • Endothelium / pathology
  • Female
  • Granulocytes / immunology*
  • Methylprednisolone / pharmacology
  • Microscopy, Fluorescence / methods
  • Neutrophils / immunology
  • Rats
  • Videotape Recording


  • Complement System Proteins
  • Methylprednisolone