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Journal of the Society for Gynecologic Investigation, Vol. 9, No. 4, 215-219 (2002)
DOI: 10.1177/107155760200900406

Interferon Gamma Antagonizes Interleukin-1ß-Induced Cyclooxygenase-2 Expression and Prostaglandin E2 Production in Human Myomaterial Cells

Frank Hertelendy, PhD, DSc

Department of Obstetrics, Gynecology and Women's Health, St. Louis University School of Medicine and St. Mary's Health Center, St. Louis, Missouri; Institute of Pathophysiology, Semmelweis University, Budapest, Hungary; Perinatology Research Branch, NICHD, Hutzel Hospital, Department of Obstetrics and Gynecology, Detroit, Michigan hertelf{at}slu.edu

Miklós Molnár, MD, PhD

Roberto Romero, MD

Department of Obstetrics, Gynecology and Women's Health, St. Louis University School of Medicine and St. Mary's Health Center, St. Louis, Missouri; Institute of Pathophysiology, Semmelweis University, Budapest, Hungary; Perinatology Research Branch, NICHD, Hutzel Hospital, Department of Obstetrics and Gynecology, Detroit, Michigan.

Objective: To evaluate the effect of interferon {gamma} (IFN{gamma}) on interleukin-1ß (IL-1) and tumor necrosis factor-{alpha} (TNF{alpha})-promoted prostaglandin E2 (PGE2) production and to investigate the interaction of IFN{gamma} and IL-1 on cyclooxygenase-2 (COX-2) expression, as well as nuclear factor-{kappa}B (NF-{kappa}B) activation in human myometrical cells.

Methods: An immortalized human myometrial cell line was cultured in Dulbecco modified Eagle medium (DMEM) fortified with 10% (v/v) fetal calf serum (FCS) in multiwell plates until near confluency. Twenty-four hours before the start of the experiments, the medium was replaced with FCS-free medium containing 0.5% bovine serum albumin. Prostaglandin E2 was determined in the medium with a specific radioimmunoassay having a sensitivity of 10 pg. The COX-2 and NF-{kappa}B inhibitory protein (I{kappa}B) protein levels were measured in cell extracts by Western blot.

Results: Cell cultures primed with IFN{gamma} produced significantly less (P < .05-.01) PGE2 in response to cytokines than cells exposed to IL-1, TNF-{alpha}, or the combination of the two. This result corresponded to a similar inhibition of I{kappa}B degradation (a prerequisite of NF-{kappa}B activation) as well as COX-2 protein steady state levels.

Conclusion: Interferon {gamma} acts as a partial antagonist of IL-1 signaling in this cell model at a site upstream from the activation of the NF-{kappa}B pathway, causing a partial inhibition of COX-2 expression and PGE2 production.

Key Words: Interleukin-1 • interferon gamma • cyclooxygenase-2 • prostaglandin E2 • myometrium


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