title: Human placental cells show enhanced production of interleukin (IL)-8 in response to lipopolysaccharide (LPS), IL-1 and tumour necrosis factor (TNF)-alpha, but not to IL-6.
abstract: Interleukin-8 (IL-8) is a chemotactic and activating factor for neutrophils which play important roles in host defence mechanisms. The human placenta constitutively produces IL-8 during pregnancy and enhances its production in chorioamnionitis. The present study was designed to investigate in vitro the regulatory mechanism for IL-8 production in the placentas in normal and inflammatory states. Placental cells produced IL-8 in a dose-dependent fashion when stimulated with lipopolysaccharide (LPS). The purified trophoblasts showed significantly higher IL-8 production than untreated placental cells. The expression of IL-8 gene in the trophoblasts in the third trimester was observed by reverse transcription-polymerase chain reaction (RT-PCR). The placental cells also release IL-8 in a dose-dependent manner, in response to r-(recombinant) IL-1alpha and tumour necrosis factor (TNF)-alpha, but not rIL-6. Moreover, LPS-activated placental cells spontaneously produced a much larger amount of IL-8 and showed increased responses to rIL-1alpha and TNF-alpha. It may, therefore, be proposed that placental cells with multiple endocrine functions exert immunological functions by constitutive production of IL-1 and TNF-alpha, which stimulate placental IL-8 release. This cytokine cascade in the placenta may be augmented by LPS in chorioamnionitis, thereby potentiating the feto-maternal defence mechanisms against infection.
authors.affiliation: Department of Obstetrics and Gynecology, Faculty of Medicine, Osaka University, 2-2 Yamada-oka, Suita City, Osaka 565-0871, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Shimoya
authors.forename: A
authors.initials: A
authors.lastname: Moriyama
authors.forename: N
authors.initials: N
authors.lastname: Matsuzaki
authors.forename: I
authors.initials: I
authors.lastname: Ogata
authors.forename: M
authors.initials: M
authors.lastname: Koyama
authors.forename: C
authors.initials: C
authors.lastname: Azuma
authors.forename: F
authors.initials: F
authors.lastname: Saji
authors.forename: Y
authors.initials: Y
authors.lastname: Murata
mesh_terms: D002478:Cells, Cultured; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism* / Q000494:pharmacology; D015850:Interleukin-6 / Q000378:metabolism* / Q000494:pharmacology; D016209:Interleukin-8 / Q000096:biosynthesis* / Q000235:genetics; D007700:Kinetics; D018950:Lipopolysaccharide Receptors / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides; D010920:Placenta / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D011247:Pregnancy; D011994:Recombinant Proteins / Q000494:pharmacology; D012016:Reference Values; D014327:Trophoblasts / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha