Aggregation of Leukocytes Induced by the Complement-Derived Peptides C3a and C5a and by Three Synthetic Formyl-Methionyl Peptides

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Abstract
The highly purified hog complement peptides C3a and C5a and three formyl-methionyl peptides induced dose-dependent aggregation of human leukocytes. For the effect Ca2+ and Mg2+ ions were required; in their absence the peptides induced specific desensitization. Human serum albumin (1 and 2%) reduced aggregation, whereas equivalent or even higher concentrations of plasma or serum were not inhibitory. SH reagents, protease inhibitors (N-tosyl-L-lysyl-chloromethyl ketone, N-tosyl-L-phenylalanyl-chloromethyl ketone), and colchicine also inhibited aggregation, whereas cytochalasin B greatly enhanced it. Dose-response studies under comparable conditions showed that aggregation is induced in similar dose ranges as chemotaxis. This suggests that complement-derived peptides generated in vivo may contribute to leukocyte accumulation in two ways, first by causing adherence of leukocytes to endothelium (equivalent to aggregation) and then by promoting migration to the inflammatory site.