title: Interleukin-1 receptor antagonist (IL-1ra) production by human amnion, chorion, and decidua.
abstract: OBJECTIVE
  This study was conducted to determine whether (1) conditioned media from unstimulated primary cultures of human amnion, chorion, or decidua contain detectable concentrations of IL-1ra in vitro, and (2) bacterial endotoxin (LPS), tumor necrosis factor-alpha (TNF-alpha), or IL-1-beta (IL-1 beta) stimulate amnion, chorion, or decidua to produce increased amounts of IL-1ra.
  
  
  METHODS
  Placentae were obtained from women at term with intact membranes before the onset of labor. Amnion, chorion, and decidual cells were isolated by standard procedures and grown to confluence. Cells were then cultured in quadruplicate for 16 h in tissue culture medium supplemented with 10% fetal calf serum or, additionally, with various concentrations of Escherichia coli LPS, TNF-alpha, or IL-1 beta. Culture supernatants were collected, and concentrations of IL-1ra were quantitated by a sensitive and specific enzyme-linked immunosorbent assay for IL-1ra.
  
  
  RESULTS
  Results showed that primary cultures of amnion and chorion from 4 of 9 and decidua from 10 of 12 placentae had detectable rates of production of IL-1ra (ranges: 0.08-6.5, 0.42-12.1, and 1.55-96.5 pg IL-1ra/microgram protein/16 h, respectively). In addition, LPS (10-1,000 ng/ml) and IL-1 beta (0.1-10 ng/ml), but not TNF-alpha (0.01-100 ng/ml), stimulated decidual cells to release/secrete increased amounts of IL-1ra compared with media alone (range: 2.5-400 pg IL-1ra/microgram protein/16 h, P < 0.0001). In contrast, neither LPS, TNF-alpha, or IL-1 beta could stimulate amnion or chorion to release/secrete IL-1ra.
  
  
  CONCLUSIONS
  These results indicate (1) that amnion, chorion, and predominantly decidua, can release or secrete IL-1ra in vitro, and (2) that LPS and IL-1 beta can stimulate decidual cells to produce increased amounts of IL-1ra.
authors.affiliation: Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan.
authors.forename: P L
authors.initials: PL
authors.lastname: Fidel
authors.forename: R
authors.initials: R
authors.lastname: Romero
authors.forename: M
authors.initials: M
authors.lastname: Ramirez
authors.forename: J
authors.initials: J
authors.lastname: Cutright
authors.forename: S S
authors.initials: SS
authors.lastname: Edwin
authors.forename: S
authors.initials: S
authors.lastname: LaMarche
authors.forename: D B
authors.initials: DB
authors.lastname: Cotton
authors.forename: M D
authors.initials: MD
authors.lastname: Mitchell
mesh_terms: D000650:Amnion / Q000187:drug effects / Q000378:metabolism*; D002823:Chorion / Q000187:drug effects / Q000378:metabolism*; D046508:Culture Techniques; D003656:Decidua / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D011247:Pregnancy; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*; D012795:Sialoglycoproteins / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D008070:Lipopolysaccharides; D017472:Receptors, Interleukin-1; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha