Elsevier

Immunology Letters

Volume 31, Issue 1, January 1992, Pages 85-90
Immunology Letters

Prostaglandin E2 inhibits the release of tumor necrosis factor-α, rather than interleukin 1β, from human macrophages

https://doi.org/10.1016/0165-2478(92)90015-GGet rights and content

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.

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    On leave from the Department of Human Microbiology, Sackler School of Medicine, Tel Aviv University, Tel-Aviv, Israel.

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