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doi:10.1016/0165-2478(92)90015-G 
Copyright © 1991 Published by Elsevier B.V.
Prostaglandin E2 inhibits the release of tumor necrosis factor-α, rather than interleukin 1β, from human macrophages
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Marien W.J.A. Fieren
, 1, Gert-Jan C.M. van den Bemd1, Shlomo Ben-Efraim2, * and Ivan L. Bonta2
Received 10 July 1991;
Abstract
We have reported previously that macrophages obtained from renal patients on continuous ambulatory peritoneal dialysis (CAPD) during an episode of infectious peritonitis display a decrease in intracellular cAMP levels and in spontaneous in vitro release of PGE2 and PGI2. Such macrophages also release large quantities of IL-1β and TNFα when stimulated in vitro by LPS. In view of the interregulatory effects between PGE2 and macrophage cytokines (IL-1β and TNFα) in their production, we examined in the present work to what extent the LPS-induced release of either IL-1β or TNFα in vitro from CAPD-originated peritoneal macrophages is affected by graded doses of exogenous PGE2 (range 0 – 1000 ng/ml) and by the cyclooxygenase inhibitor indomethacin (INDO) (10−6 M). IL-1β and TNFα were determined using an enzyme-linked immunoabsorbent assay and an immunoradiometric assay, respectively. We found that PGE2 invariably induced a dose-dependent decrease in TNFα release. In peritoneal macrophages collected during an infection-free period, TNFα release decreased from 3225 pg/ml (controls) to 353 pg/ml at 1000 ng/ml of PGE2, and in peritoneal macrophages collected during an episode of infectious peritonitis, it decreased from 4100 pg/ml (controls) to 545 pg/ml at 100 ng/ml of PGE2. However, PGE2 failed to influence the secretion of IL-1β. INDO induced an approx, two-fold increase in TNFα release, but had no effect on IL-1β release. These findings indicate that exogenous and endogenous PGE2 controls the release of TNFα rather than IL-1β from LPS-stimulated peritoneal macrophages.
Keywords: Tumor necrosis factor α; Interleukin-1β; Prostaglandin E2; LPS, bacterial lipopolysaccharide; Indomethacin; Macrophage, peritoneal human
Correspondence to: Marien W. J. A. Fieren, Department of Internal Medicine I, University Hospital “Dijkzigt”, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.* On leave from the Department of Human Microbiology, Sackler School of Medicine, Tel Aviv University, Tel-Aviv, Israel.
