Modulation of phagocytosis by and lysosomal enzyme secretion from guinea-pig neutrophils: effect of nonsteroid anti-inflammatory agents and prostaglindins.

Guinea-pig neutrophils released lysosome granule-associated beta-glucuronidase, but not cytoplasmic lactate dehydrogenase during cell contact with and phagocytosis of serum-treated zymosan particles. Naproxen, chloroquine and indomethacin inhibited particle uptake by and lysosomal enzyme secretion from neutrophils incubated with zymosan in Krebs-Ringer phosphate medium, pH 7.4, at 37 degrees C. Acetylsalicyclic acid, fenoprofen and ibuprofen were inactive. Prostaglandins (PG) E1, E2, A1, A2, B1 and B2 reduced particle ingestion by and discharge of lysosomal enzymes from neutrophils. PGF2alpha accelerated lysosomal enzyme release, had no effect on phagocytosis at high concentrations and inhibited both processes at low concentrations.. PGF1alpha was inactive. In the presence of cytochalasin B, an agent which inhibits phagocytosis while havine no effect on selective lysosomal enzyme secretion, naproxen, chloroquine and indomethacin, continued to inhibit the discharge of beta-glucuronidase from neutrophils. PGE1, PGE2, PGA1, PGA2, PGB1 and PGB2 reduced lysosomal enzyme release from cytochalasin B-treated neutrophils. PGF2alpha accelerated at high and inhibited at low concentrations the selective secretion of beta-glucuronidase from cytochalasin B-treated neutrophils. PGF1alpha was again inactive. These studies indicated that guinea-pig neutrophils are capable of a selective release of lysosomal enzymes (beta-glucuronidase) during ingestion of serum-treated zymosan particles and that certain anti-inflammatory drugs and prostaglansins may function as modulators of the phagocytic release of lysosomal enzymes from neutrophils.