title: Prostaglandin production by human chorion laeve cells in response to inflammatory mediators.
abstract: Cytokines produced during an intrauterine infection may cause increased prostaglandin production and thus preterm labor. Previously, we have shown that cytokines increase prostaglandin production by human amnion and decidual cells. In the present study we examined the effect of interleukin-1 beta (IL-1 beta), tumor necrosis factor (TNF), and endotoxin on prostaglandin production by chorion laeve cells. Upon reaching confluence at day 3 and after 10 days in culture, human chorion laeve cells in primary culture were incubated with each substance. On day 3 of culture the chorion cells demonstrated limited responsiveness to the test agents with a maximum response of less than two times basal production. However, after 10 days the cultures were highly responsive to the test agents with maximum responses of greater than ten times basal production. We conclude that early in culture chorion cells may express fewer functional receptors for the test agents. Alternatively, a subpopulation of chorion cells responsive to cytokines and endotoxin may predominate by day 10 of culture. Chorion laeve, therefore, could contribute to the increased intrauterine prostaglandin production associated with infection-driven preterm labor.
authors.affiliation: Department of Obstetrics and Gynecology, University of Utah Medical Center, Salt Lake City 84132.
authors.forename: S
authors.initials: S
authors.lastname: Lundin-Schiller
authors.forename: M D
authors.initials: MD
authors.lastname: Mitchell
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism*; D002478:Cells, Cultured / Q000187:drug effects; D002823:Chorion / Q000166:cytology / Q000378:metabolism*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism*; D015232:Dinoprostone / Q000031:analogs & derivatives / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000494:pharmacology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism*; D007375:Interleukin-1 / Q000494:pharmacology; D011247:Pregnancy; D015230:Prostaglandin D2 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D004731:Endotoxins; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D015121:6-Ketoprostaglandin F1 alpha; C025088:11-deoxy-15-keto-13,14-dihydro-11 beta,16-cycloprostaglandin E2; D015237:Dinoprost; D015232:Dinoprostone; D015230:Prostaglandin D2