title: Omega-3 fatty acids and decidual cell prostaglandin production in response to the inflammatory cytokine IL-1beta.
abstract: OBJECTIVE
  The objective of this study was to determine the effect of omega-3 fatty acids (eicosapentaenoic acid [EPA]; docosahexaenoic acid [DHA]) on prostaglandin production and prostanoid enzyme expression in cultured decidual cells exposed to interleukin-1beta (IL-1beta), a cytokine that plays a major role in inflammation.
  
  
  METHODS
  Decidua was obtained from human placentas of nonlaboring patients at term cesarean delivery (N = 6) and cultured by using standard cell culture techniques. Cells were preincubated in defined media with various concentrations of vehicle, DHA, or EPA for 1 hour. IL-1beta (10 ng/mL) was then added to the media, and experiments were terminated 12 hours after exposure to IL-1beta. Prostaglandin E2 (PGE2) and PGF2alpha concentrations in conditioned media were measured by enzyme-linked immunosorbent assay; cyclooxygenase-1 (COX-1), COX-2, microsomal prostaglandin E synthase (mPGES)-1, mPGES-2, and 15-hydroxy prostaglandin dehydrogenase (PGDH) expression were quantified by real-time polymerase chain reaction and immunoblotting. Groups were compared with the use of Student t test, with significance defined as P < .05.
  
  
  RESULTS
  Preincubation with DHA decreased prostaglandin production by up to 80% when compared with controls. DHA decreased both mPGES-1 and -2 messenger RNA expression by approximately 50% (P = .02). Preincubation in DHA or EPA had no effect on COX-1, COX-2, and PGDH messenger RNA or protein expression.
  
  
  CONCLUSIONS
  Under conditions simulating inflammation, supplementation with omega-3 fatty acids decreases PGE2 and PGF2alpha production in cultured decidual cells. The reduction in prostaglandin production was associated with a decreased expression of mPGES-1 and -2. These findings suggest a mechanism by which omega-3 fatty acid supplementation decreases the incidence of preterm birth in high-risk patients.
authors.affiliation: Obstetrics and Gynecology, NYU School of Medicine, New York, NY, USA.
authors.forename: Ashley S
authors.initials: AS
authors.lastname: Roman
authors.forename: Jeremy
authors.initials: J
authors.lastname: Schreher
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Mackenzie
authors.forename: Peter W
authors.initials: PW
authors.lastname: Nathanielsz
mesh_terms: D002478:Cells, Cultured; D003656:Decidua / Q000166:cytology / Q000378:metabolism*; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000494:pharmacology*; D019746:Intramolecular Oxidoreductases / Q000235:genetics; D008861:Microsomes / Q000201:enzymology; D011247:Pregnancy; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D000071876:Prostaglandin-E Synthases; D011453:Prostaglandins / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000037:antagonists & inhibitors
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D012333:RNA, Messenger; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; D019746:Intramolecular Oxidoreductases; C000605862:PTGES protein, human; C000605863:PTGES2 protein, human; D000071876:Prostaglandin-E Synthases