Abstract
Human PMNs release prostaglandins E and F to the surrounding medium when these cells are exposed to zymosan. PGE1 is the prostaglandin compound found in highest concentration in the medium, and the PGE/PGF balance is approximately 3∶1. Release of prostaglandins is not due to platelet contamination. Agents which inhibit prostaglandin synthesis (indomethacin, aspirin) prevent release of prostaglandins from phagocytic cells. Addition to cells of dibutyryl cyclic 3′,5′-adenosine monophosphate produces striking increases in concentrations of prostaglandins released during ingestion of zymosan. Prostaglandins appear to be synthesized by human PMN during phagocytosis, and their release from cells may help regulate the inflammatory response.
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Supported by a grant from the University of Connecticut Research Foundation, by NIH Grant AM 17309, and a Clinical Center Grant of the Arthritis Foundation.
Abbreviations used in this paper: CB, cytochalasin B; dbcAMP, dibutyryl cyclic 3′,5′-adenosine monophosphate; LDH, lactic acid dehydrogenase; PGE and PGF, prostaglandins E and F; PMN, polymorphonuclear leukocytes; and TLC, thin-layer chromatography.
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Zurier, R.B., Sayadoff, D.M. Release of prostaglandins from human polymorphonuclear leukocytes. Inflammation 1, 93–101 (1975). https://doi.org/10.1007/BF00918062
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DOI: https://doi.org/10.1007/BF00918062