title: Eicosapentaenoic acid is more effective than docosahexaenoic acid in inhibiting proinflammatory mediator production and transcription from LPS-induced human asthmatic alveolar macrophage cells.
abstract: OBJECTIVE
  The purpose of the study was to determine which of the active constituents of fish oil, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), is most effective in suppressing proinflammatory mediator generation and cytokine expression from LPS-stimulated human asthmatic alveolar macrophages (AMphi).
  
  
  METHODS
  The AMphi were obtained from twenty-one asthmatic adults using fiberoptic bronchoscopy. Cells were pretreated with DMEM, pure EPA, an EPA-rich media (45% EPA/10% DHA), pure DHA, a DHA-rich media (10% EPA/50% DHA) or Lipovenos (n-6 PUFA), and then exposed to Dulbecco's Modified Eagle's Medium (DMEM) (-) or LPS (+). Supernatants were analyzed for leukotriene (LT)B(4), prostaglandin (PG)D(2), tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta production. Detection of TNF-alpha and IL-1beta mRNA expression levels was quantified by reverse transcriptase polymerase chain reaction.
  
  
  RESULTS
  120 microM pure EPA and EPA-rich media significantly (p<0.05) suppressed TNF-alpha and IL-1beta mRNA expression and the production of LTB(4), PGD(2) and TNF-alpha and IL-1beta in LPS-stimulated primary AMphi cells obtained from asthmatic patients to a much greater extent than 120 microM pure DHA and DHA-rich media respectively.
  
  
  CONCLUSIONS
  This study has shown for the first time that EPA is a more potent inhibitor than DHA of inflammatory responses in human asthmatic AMphi cells.
authors.affiliation: Exercise Biochemistry Laboratory, Department of Kinesiology, Indiana University, Bloomington, IN 47401, USA. tmickleb@indiana.edu
authors.forename: Timothy D
authors.initials: TD
authors.lastname: Mickleborough
authors.forename: Sandra L
authors.initials: SL
authors.lastname: Tecklenburg
authors.forename: Gregory S
authors.initials: GS
authors.lastname: Montgomery
authors.forename: Martin R
authors.initials: MR
authors.lastname: Lindley
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001249:Asthma / Q000276:immunology*; D002460:Cell Line; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000517:prevention & control*; D053583:Interleukin-1beta / Q000378:metabolism; D007975:Leukotriene B4 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D016676:Macrophages, Alveolar / Q000187:drug effects* / Q000502:physiology*; D015230:Prostaglandin D2 / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007975:Leukotriene B4; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; D015230:Prostaglandin D2