Complement (C5-a)-induced granulocyte aggregation in vitro. A possible mechanism of complement-mediated leukostasis and leukopenia.
Activated plasma complement will induce biphasic aggregation of human granulocytes dectable by standard nephelometric techniques. The responsible active component was suggested to be C5a by molecular weight and heat-stability assays; moreover, aggragating activity was ablated by anti-C5 but not anti-C3 antibodies. C5a prepared by trypsinization of purified C5 reproduced the aggregating activity of whole activated plasma, whereas plasma from a C5-deficient donor did not support aggregation. Embolization of granulocyte aggregates might be a previously unsuspected cause of leukostasis and pulmonary damage in various clinical situations where intravascular complement activation occurs.
D002449:Cell Aggregation; D003182:Complement C5 / Q000172:deficiency / Q000378:metabolism; D003165:Complement System Proteins / Q000378:metabolism; D006098:Granulocytes / Q000502:physiology*; D006487:Hemostasis; D006801:Humans; D007962:Leukocytes / Q000502:physiology*; D007970:Leukopenia / Q000276:immunology*; D008854:Microscopy, Electron; D011652:Pulmonary Circulation; D015054:Zymosan / Q000494:pharmacology
D003182:Complement C5; D003165:Complement System Proteins; D015054:Zymosan