title: LPS mediated production of IL-1, PGE2 and PGF2alpha from term decidua involves tumour necrosis factor and tumour necrosis factor receptor p55.
abstract: Prostaglandins, with cytokines involved as intermediate factors, may have an essential role in premature labour when infection is present. We therefore wanted to study tumour necrosis factor (TNF), in cytokine and prostaglandin production in reproductive tissue. Decidual cell cultures were established and cells were stimulated with lipopolysaccharides (LPS). Media concentrations of TNF, interleukin-1 (IL-1), IL-6 and prostaglandin E2 and F2alpha were analysed, and involvement of LPS receptor CD14, TNF and TNF receptors (p55 and p75) were analysed, by studying effects after administration of specific antibodies. LPS induced an early peak elevation of TNF, with a subsequent release of IL-1, IL-6 and prostaglandins. Antibodies against CD14 inhibited these LPS effects. TNF antibodies reduced production of IL-1 and prostaglandins, whereas no significant influence on IL-6 production was observed. Antibodies against the TNF receptor p55 reduced all observed TNF effects. In contrast, p75 antibodies did not influence cytokine or prostaglandin production in this system. Our results suggest that increased TNF production is a prerequisite for LPS stimulated production of IL-1 and prostaglandins from decidual cells. LPS may directly stimulate IL-6 production. Of the two TNF receptors studied, only p55 seemed to be involved in the TNF signal transduction.
authors.affiliation: Institute of Cancer Research and Molecular Biology, Norwegian University of Science and Technology, Trondheim. knut.j.arntzen@medisin.ntnu.no
authors.forename: K J
authors.initials: KJ
authors.lastname: Arntzen
authors.forename: K
authors.initials: K
authors.lastname: Egeberg
authors.forename: S
authors.initials: S
authors.lastname: Rahimipoor
authors.forename: L
authors.initials: L
authors.lastname: Vatten
authors.forename: R
authors.initials: R
authors.lastname: Austgulen
mesh_terms: D015703:Antigens, CD / Q000276:immunology*; D002478:Cells, Cultured; D003656:Decidua / Q000187:drug effects / Q000276:immunology*; D015237:Dinoprost / Q000276:immunology*; D015232:Dinoprostone / Q000276:immunology*; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D011247:Pregnancy; D018124:Receptors, Tumor Necrosis Factor / Q000276:immunology*; D047888:Receptors, Tumor Necrosis Factor, Type I; D015398:Signal Transduction / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D015703:Antigens, CD; D007375:Interleukin-1; D008070:Lipopolysaccharides; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha; D015237:Dinoprost; D015232:Dinoprostone