Intrauterine infection and the effects of inflammatory mediators on prostaglandin production by myometrial cells from pregnant women

Byline: Jeffrey K. Pollard, Murray D. Mitchell Keywords: Prostaglandins; myometrium; cytokines; intrauterine infection Abstract: OBJECTIVE: Our purpose was to evaluate the effects of known stimulants of prostaglandin production on cultured myometrial cells from women in labor with and without intrauterine infection. STUDY DESIGN: Myometrial segments were obtained from 16 patients between 33 and 40 weeks' gestation who had been in labor for [greater than or equal to]8 hours at cesarean delivery; 8 patients had clinical chorioamnionitis and 8 did not. Myometrial cells were isolated and grown in culture. Incubations were conducted with interleukin-1[beta], tumor necrosis factor-[alpha], or epidermal growth factor. Prostaglandin E.sub.2, prostaglandin F.sub.2[alpha], and 6-keto-prostaglandin F.sub.1[alpha] (the stable metabolite of prostacyclin) were measured by radioimmunoassay, and cellular protein was determined. RESULTS: Cultured myometrial cells from patients with and without prior intrauterine infection produced prostaglandins in response to interleukin-1[beta], tumor necrosis factor-[alpha], and epidermal growth factor at a significantly increased rate (p < 0.05 vs controls at and above 10 ng/ml of interleukin-1[beta], tumor necrosis factor-[alpha], and epidermal growth factor). The major prostaglandin produced in response to each stimulant was 6-keto-prostaglandin F.sub.1[alpha]; however, this response was attenuated in cells from patients with intrauterine infection. CONCLUSIONS: Cultured human myometrial cells from patients with and without prior intrauterine infection respond to known stimulants of prostaglandin production. Prior intrauterine infection has no effect on baseline prostaglandin production, but the amount of prostacyclin produced as a response to cellular stimulants is decreased with prior intrauterine infection. This effect may have a role in regulating myometrial function in intrauterine infection. (AM J OBSTET GYNECOL 1996;174:682-6.) Author Affiliation: Salt Lake City, Utah Article History: Received 10 November 1994; Revised 11 April 1995; Accepted 16 June 1995 Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, University of Utah., [star][star] Reprint requests: Jeffrey K. Pollard, MD, Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Vermont, Burlington, VT 05401., a 0002-9378/96 $5.00 + 0 6/1/67237