title: Prostaglandin and cytokine release by trophoblastic villi.
abstract: Trophoblastic villi may have several protective mechanisms against the maternal immune system. They do not display major human leukocyte antigen antigens, and therefore a T cell-mediated response is unlikely. The syncytiotrophoblast provides a seamless coating, and the microvilli on its surface represent a very large surface area which has a high capacity for absorbing antibody. The syncytiotrophoblast also contains inhibitors of complement. Although these mechanisms are essential, they may not be sufficient protection. An additional mechanism by which the trophoblast could control its immediate environment in the decidua or maternal blood may be through the release of prostaglandins (PG) and cytokines. This possibility has been investigated here by measuring PG and several cytokines released from first trimester trophoblastic villi cultured for 24 h. PGE is the main primary prostaglandin with a release of 240 +/- 95 pg/mg/24 h. There was an extensive accompanying production of metabolites (13,14-dihydro-15-keto PGF, 2.4 +/- 0.4 ng/mg/24 h, and 13,14-dihydro-15-keto PGE, 0.61 +/- 0.11 ng/mg/24 h). Cytokines were measured in culture fluid by specific enzyme-linked immunosorbent assays. Interleukin (IL)-2 and IL-10 release were not detectable, but IL-1 beta (5.2 +/- 1.1 pg/mg/24 h) and tumour necrosis factor (TNF) alpha (2.3 +/- 0.5 pg/mg/24 h) were found to be accompanied by much higher concentrations of inhibitors, IL-1 receptor antagonist (200 +/- 44 pg/mg/24 h) and soluble receptors for TNF types I (19.5 +/- 1.6 pg/mg/24 h) and II (19.3 +/- 2.8 pg/mg/24 h). Because PGE can influence the function of many leukocytes by raising intracellular cAMP concentrations, the release of humoral factors from the villous trophoblast might be important in pregnancy maintenance.
authors.affiliation: Department of Obstetrics and Gynaecology, Centre for Reproductive Biology, Edinburgh, UK.
authors.forename: R W
authors.initials: RW
authors.lastname: Kelly
authors.forename: G G
authors.initials: GG
authors.lastname: Carr
authors.forename: C L
authors.initials: CL
authors.lastname: Elliott
authors.forename: M
authors.initials: M
authors.lastname: Tulppala
authors.forename: H O
authors.initials: HO
authors.lastname: Critchley
mesh_terms: D002824:Chorionic Villi / Q000276:immunology* / Q000378:metabolism*; D017077:Culture Media, Conditioned; D046508:Culture Techniques; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000378:metabolism; D011247:Pregnancy; D011255:Pregnancy Maintenance / Q000502:physiology; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D012795:Sialoglycoproteins / Q000378:metabolism; D014327:Trophoblasts / Q000276:immunology* / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D017077:Culture Media, Conditioned; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D011453:Prostaglandins; D011458:Prostaglandins E; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha