Neutrophil aggregation and degranulation. Effect of arachidonic acid

Abstract

In response to aggregating and degranulating stimuli, platelets metabolize endogenous arachidonic acid to bioactive derivatives. These derivatives can stimulate platelets to degranulate and aggregate and, therefore, may be mediators of the platelet response. Because exogenous arachidonic acid also stimulates platelets to degranulate, aggregate, and form these mediators, we examined the effect of adding arachidonic acid to purified human neutrophil suspensions. Micromolar concentrations of arachidonic acid stimulated neutrophils to aggregate but not to degranulate. Cytochalasin B, a potentiator of neutrophil responses to chemotactic factors, also potentiated the arachidonic-acid-induced aggregation response; 5,8,11,14-eicosatetraynoic acid, an inhibitor of arachidonic acid metabolism, blocked this response. Aggregation of neutrophils, was not stimulated by several fatty acids with structural similarity to arachidonic acid. These results suggest that metabolic derivatives of arachidonic acid may be active in stimulating certain neutrophil responses. The role of these derivatives in mediating neutrophil responses to various stimuli needs to be examined.