title: Aspirin differentially regulates endotoxin-induced IL-12 and TNF-alpha production in human dendritic cells.
abstract: OBJECTIVE
  In the development of autoimmune diseases, dendritic cells (DC) play critical roles. Here, we examined the effect of aspirin on lipopolysaccharide (LPS)-induced DC activation.
  
  
  METHODS
  The monocyte-derived DC were established. The cytokine production was measured by ELISA, reverse transcriptase/polymerase chain reaction, or intracellular staining analyzed by flow cytometry. The expression of cell surface molecules was determined by flow cytometry.
  
  
  RESULTS
  Aspirin inhibited LPS-induced DC maturation and costimulatory molecules expression. Aspirin, at therapeutic concentrations, also decreased LPS-induced IL-12 and IL-10 production. In contrast, the LPS-induced TNF-alpha production was enhanced by aspirin. The differential effects of aspirin on IL-12 and TNF-alpha production may not be due to down-regulation of cyclooxygenase activities.
  
  
  CONCLUSIONS
  The various effects of aspirin on LPS-stimulated DC may influence the understanding of the diverse immunomodulatory mechanisms of this anti-inflammatory drug.
authors.affiliation: Rheumatology/Immunology and Allergy, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
authors.forename: L J
authors.initials: LJ
authors.lastname: Ho
authors.forename: D M
authors.initials: DM
authors.lastname: Chang
authors.forename: H Y
authors.initials: HY
authors.lastname: Shiau
authors.forename: C H
authors.initials: CH
authors.lastname: Chen
authors.forename: T Y
authors.initials: TY
authors.lastname: Hsieh
authors.forename: Y L
authors.initials: YL
authors.lastname: Hsu
authors.forename: C S
authors.initials: CS
authors.lastname: Wong
authors.forename: J H
authors.initials: JH
authors.lastname: Lai
mesh_terms: D001241:Aspirin / Q000494:pharmacology*; D001483:Base Sequence; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000187:drug effects* / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D006801:Humans; D016753:Interleukin-10 / Q000032:analysis / Q000096:biosynthesis*; D018664:Interleukin-12 / Q000032:analysis / Q000096:biosynthesis*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008969:Molecular Sequence Data; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000096:biosynthesis*; D015854:Up-Regulation
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D001241:Aspirin