Stimulation of human neutrophil degranulation with 1-0-octadecyl-2-0-acetyl-sn-glyceryl-3-phosphorylcholine: Modulation by inhibitors of arachidonic acid metabolism

1-0-octadecyl-2-0-acetyl-sn-glyceryl-3-phosphorylcholine (C₁₈-AGEPC) stimulated a concentration (10-¹⁰-10-⁶M)-dependent release of granule-associated enzymes from human neutrophils. Cells which were not preincubated with cytochalasin B prior to exposure to C₁₈-AGEPC did not degranulate. C₁₈-AGEPC-elicited enzyme release was significantly reduced, but not abolished, in the absence of extracellular calcium. The lipoxygenase inhibitor, nordihydroguaiaretic acid and the lipoxygenase/cyclo-oxygenase inhibitor, 5,8,11,14-eicosatetraynoic acid, an acetylenic analog of arachidonic acid, caused a concentration-dependent suppression of enzyme discharge from neutrophils exposed to C₁₈-AGEPC. However, the cyclo-oxygenase inhibitors, indomethacin, ibuprofen and flurbiprofen had no effect on C₁₈-AGEPC-induced enzyme extrusion.