Monocyte aggregation and superoxide anion release in response to formyl-methionyl-leucyl-phenylalanine (FMLP) and platelet-activating factor (PAF).

Like the PMN, human peripheral blood monocytes were capable of aggregating in response to FMLP and PAF. Monocyte aggregation was dependent on glycolysis and the presence of divalent cations. Unlike the PMN, monocyte aggregation in response to FMLP was not accompanied by degranulation, nor was it potentiated by cytochalasin B. Furthermore, cytochalasin B and its cogenitor, dihydrocytochalasin B, inhibited aggregation in response to PAF. PAF and FMLP appeared to react with the monocyte at separate receptors because sequential challenge of the monocyte with the same agents failed to elicit further aggregation, whereas rechallenge with the alternative agent induced further aggregation. Because the monocyte will aggregate to chemotactic agents in vitro, it is likely that the cell will be affected by these agents in vivo, which could lead to leukoembolization of circulating monocytes.