V J Goodwin1, T A Sato, M D Mitchell, J A Keelan. 1. Department of Pharmacology and Clinical Pharmacology, Faculty of Medicine and Health Science, University of Auckland School of Medicine, New Zealand.
Abstract
PROBLEM: To determine the effects of anti-inflammatory cytokines on the production of inflammatory mediators by placental cells. METHOD OF STUDY: Cells from term human placentas were isolated and cultured in vitro in the presence of anti-inflammatory cytokines interleukin (IL)-4, IL-10, and transforming growth factor (TGF)-beta. Their effects on the production of IL-8 and prostaglandin E2 (PGE2) were investigated under basal conditions and after stimulation with IL-1 beta and tumor necrosis factor (TNF)-alpha. RESULTS: Both IL-10 and IL-4 inhibited IL-1 beta- and TNF-alpha-induced PGE2 production but had no significant effects on the production of PGE2 under basal conditions. TGF-beta 1 was without effect in stimulated cells, whereas under basal conditions TGF-beta 1 stimulated PGE2 production. Similar trends were seen for IL-8 production, with the exceptions that TGF-beta 1 decreased the TNF-alpha-induced production and IL-4 decreased basal IL-8 production. CONCLUSIONS: The anti-inflammatory effects shown by IL-4, IL-10, and (to lesser extent) TGF-beta may play a role in ameliorating the potentially harmful effects of pro-inflammatory mediators in the feto-placental unit.
PROBLEM: To determine the effects of anti-inflammatory cytokines on the production of inflammatory mediators by placental cells. METHOD OF STUDY: Cells from term human placentas were isolated and cultured in vitro in the presence of anti-inflammatory cytokines interleukin (IL)-4, IL-10, and transforming growth factor (TGF)-beta. Their effects on the production of IL-8 and prostaglandin E2 (PGE2) were investigated under basal conditions and after stimulation with IL-1 beta and tumor necrosis factor (TNF)-alpha. RESULTS: Both IL-10 and IL-4 inhibited IL-1 beta- and TNF-alpha-induced PGE2 production but had no significant effects on the production of PGE2 under basal conditions. TGF-beta 1 was without effect in stimulated cells, whereas under basal conditions TGF-beta 1 stimulated PGE2 production. Similar trends were seen for IL-8 production, with the exceptions that TGF-beta 1 decreased the TNF-alpha-induced production and IL-4 decreased basal IL-8 production. CONCLUSIONS: The anti-inflammatory effects shown by IL-4, IL-10, and (to lesser extent) TGF-beta may play a role in ameliorating the potentially harmful effects of pro-inflammatory mediators in the feto-placental unit.
Authors: Craig C Davis; Luciana C Marti; Gregory D Sempowski; Durairaj A Jeyaraj; Paul Szabolcs Journal: Cancer Res Date: 2010-06-08 Impact factor: 12.701