MODULATION OF PHAGOCYTOSIS BY AND LYSOSOMAL ENZYME-SECRETION FROM GUINEA-PIG NEUTROPHILS - EFFECT OF NONSTEROID ANTI-INFLAMMATORY AGENTS AND PROSTAGLANDINS

  • 1 January 1977
    • journal article
    • research article
    • Vol. 200  (3) , 647-657
Abstract
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.degree. 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. PGF2.alpha. accelerated lysosomal enzyme release, had no effect on phagocytosis at high concentrations and inhibited both processes at low concentrations. PGF1.alpha. was inactive. In the presence of cytochalasin B, an agent which inhibits phagocytosis while having 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. PGF2.alpha. accelerated at high and inhibited at low concentrations the selective secretion of .beta.-glucuronidase from cytochalasin B-treated neutrophils. PGF1.alpha. was again inactive. Guinea-pig neutrophils are apparently capable of a selective release of lysosomal enzymes (.beta.-glucuronidase) during ingestion of serum-treated zymosan particles and certain anti-inflammatory drugs and prostaglandins may function as modulators of the phagocytic release of lysosomal enzymes from neutrophils.

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