A possible role of arachidonic acid in human neutrophil aggregation and degranulation.
Chemotactic factors stimulate neutrophils to aggregate and, in the presence of cytochalasin B, to degranulate. Recently, the authors found that arachidonic acid also stimulates human neutrophils to aggregate but does not stimulate cytochalasin-B-treated or untreated cells to degranulate. In this report the authors examined the effect of three blockers of arachidonic acid metabolism on these cellular responses. It was found that the arachidonic acid analog 5,8,11,14-eicosatetraynoic acid and indomethacin, but not aspirin, inhibited no only the arachidonic-acid-induced aggregation response but also the degranulation responses evoked  by C5a or a synthetic oligopeptide chemotactic factor. These results suggest that arachidonic acid may be a precursor of bioactive metabolites that stimulate the aggregation and foster the degranulation responses of neutrophils. Thus, these metabolites may be mediators of neutrophil function. Agents that block their formation may thereby inhibit aggregation and degranulation.
D015117:5,8,11,14-Eicosatetraynoic Acid / Q000494:pharmacology; D001095:Arachidonic Acids / Q000378:metabolism / Q000502:physiology*; D001241:Aspirin / Q000494:pharmacology; D002465:Cell Movement / Q000187:drug effects; D003594:Cytoplasmic Granules / Q000648:ultrastructure; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000648:ultrastructure*
D001095:Arachidonic Acids; D015117:5,8,11,14-Eicosatetraynoic Acid; D001241:Aspirin; D007213:Indomethacin