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Enhanced prostaglandin E 2 and thromboxane B 2 release from resident peritoneal macrophages isolated from morphine‐dependent rats
Author(s) -
Elliott G.R.,
van Batenburg M.J.,
Dzoljic M.R.
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)81231-0
Subject(s) - morphine , prostaglandin e2 , chemistry , prostaglandin , phagocytosis , endocrinology , prostaglandin e , eicosanoid , thromboxane b2 , medicine , in vitro , macrophage , secretion , thromboxane , pharmacology , enzyme , biochemistry , immunology , platelet , arachidonic acid
Resident peritoneal macrophages from morphine‐addicted rats (4 days) released more prostaglandin (PG) E 2 and thromboxane (Tx) B 2 , but not 6‐keto‐PGF 1a , than cells from control animals. This effect, which was due to an enhancement of endogenous AA turnover, was not related to any changes in cAMP synthesis or lysososomal enzyme secretion. [D‐Ala 2 ]‐Met‐enkephalin had no effect on eicosanoid release in vitro. Both morphine and PGE 2 have been shown to depress macrophage functions. We suggest that morphine‐stimulated macrophage PGE 2 synthesis, and the consequent inhibition of phagocytosis, could contribute to the decreased resistance to infections associated with opiate addiction.