title: Intrauterine infection and the effects of inflammatory mediators on prostaglandin production by myometrial cells from pregnant women.
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.
  
  
  METHODS
  Myometrial segments were obtained from 16 patients between 33 and 40 weeks' gestation who had been in labor for > or = 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 E2, prostaglandin F2 alpha, and 6-keto-prostaglandin F1 alpha (the stable metabolite of prostacyclin) were measured by radioimmunoassay, and cellular protein was determined.
  
  
  RESULTS
  Cultured human 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 F1 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.
authors.affiliation: Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, USA.
authors.forename: J K
authors.initials: JK
authors.lastname: Pollard
authors.forename: M D
authors.initials: MD
authors.lastname: Mitchell
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D002478:Cells, Cultured; D016207:Cytokines / Q000494:pharmacology*; D015237:Dinoprost / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D004815:Epidermal Growth Factor / Q000494:pharmacology; D005260:Female; D006801:Humans; D007239:Infections / Q000378:metabolism*; D007375:Interleukin-1 / Q000494:pharmacology; D009215:Myometrium / Q000378:metabolism*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014591:Uterine Diseases / Q000378:metabolism*
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D011453:Prostaglandins; D014409:Tumor Necrosis Factor-alpha; D015121:6-Ketoprostaglandin F1 alpha; D004815:Epidermal Growth Factor; D015237:Dinoprost; D015232:Dinoprostone