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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 12 4645-4651
Copyright © 1999 by The Endocrine Society

Original Studies

Interleukin-10 Modifies the Effects of Interleukin-1ß and Tumor Necrosis Factor-{alpha} on the Activity and Expression of Prostaglandin H Synthase-2 and the NAD+-Dependent 15-Hydroxyprostaglandin Dehydrogenase in Cultured Term Human Villous Trophoblast and Chorion Trophoblast Cells1

F. Pomini2, A. Caruso and J. R. G. Challis

Medical Research Council Group in Fetal and Neonatal Health and Development, Department of Physiology, and Obstetrics and Gynecology, University of Toronto (F.P., J.R.G.C.), Toronto, Ontario, Canada M4Y 1M8; and the Department of Obstetrics and Gynecology, Universita Cattolica del Sacro Cuore (F.P., A.C.), Rome 00168, Italy

Address all correspondence and requests for reprints to: Dr. F. Pomini, Universita Cattolica del Sacro Cuore, Department of Obstetrics and Gynecology, L.go A. Gemelli No. 8, Rome 00168, Italy. E-mail: fpomini{at}mix.it

The concentrations of tumor necrosis factor-{alpha} (TNF{alpha}) and interleukin-1ß (IL-1ß), two inflammatory cytokines in amniotic fluid, have been shown to rise during chorioamnionitis. This is probably related to activation of the immune system in order to intensify the inflammatory process and to protect the maternal and fetal organism from infectious agents. These cytokines activate the PG biosynthetic pathway in several tissues, but few studies have examined effects on PG-metabolizing enzymes. When PGs are produced by increased synthesis and/or decreased metabolism at the chorio-decidual interface, labor can be induced. Interleukin-10 (IL-10) is known to act as an antiinflammatory cytokine. The goals of this study were to evaluate the interaction of IL-10 with IL-1ß and TNF{alpha} on PG synthesis and to determine the effects of IL-10, IL-1ß, and TNF{alpha} on PG metabolism using purified cultures of villous trophoblast and chorion trophoblast cells prepared from placentas of patients at term. Cells were treated with IL-1ß and TNF{alpha} with or without IL-10 for various times up to 24 h. Levels of messenger ribonucleic acid (mRNA) encoding PGH synthase-2 (PGHS-2) and NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) were quantified by Northern blotting, and PGE2 and 13,14-dihydro-15-keto-PGF2{alpha} (PGFM) output in the medium was measured by RIA. IL-1ß increased PGHS-2 mRNA and PGE2 output from villous and chorion trophoblasts and decreased PGDH mRNA in villous trophoblasts (all P < 0.05). These effects were reversed by IL-10. We found no change in PGHS-2 mRNA or PGE2 output in either trophoblast type treated with TNF{alpha}, but TNF{alpha} reduced PGDH mRNA in villous trophoblast, and this effect was reversed by IL-10 (both P < 0.05). We conclude that proinflammatory cytokines can influence PG output through effects on PG synthesis and metabolism and that these effects may be opposed by an antiinflammatory cytokine. These interactions may be important in the progression of preterm labor with underlying infection and in term labor in regions of the uterus where cytokine production is increased.




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