Effect of prostaglandins E1, E2 and F2alpha on neutrophil aggregation.
Recently we have found that chemotactic factors stimulate neutrophils in suspension to aggregate. Because of an obvious analogy to platelet aggregation, we examined the influence of three prostaglandins on this process. Prostaglandins E1, E2 and F2alpha alone did not cause aggregation of the neutrophils but were able to partially inhibit the aggregation response induced by the synthetic chemotactic tripeptide, formyl-methionyl-leucyl-phenylalanine. The minimal inhibitory concentrations for prostaglandins E1, E2 and F2alpha were 10(-7), 10(-6) and 10(-5)M, respectively. These results are similar to those found for the prostaglandin-induced inhibition of platelet aggregation. It may be, therefore, that neutrophil aggregation, like platelet aggregation, is modulated by intracellular prostaglandins and other products of arachidonic acid metabolism.
D002449:Cell Aggregation / Q000187:drug effects; D006801:Humans; D009504:Neutrophils / Q000187:drug effects*; D010649:Phenylalanine / Q000031:analogs & derivatives; D011458:Prostaglandins E / Q000008:administration & dosage / Q000494:pharmacology*; D011460:Prostaglandins F / Q000008:administration & dosage / Q000494:pharmacology*; D013997:Time Factors
D011458:Prostaglandins E; D011460:Prostaglandins F; D010649:Phenylalanine