title: [Production of interleukin-11 in human gingival fibroblasts stimulated with IL-1alpha and tumor necrosis factor-alpha].
abstract: OBJECTIVE
  To investigate what role IL-11 plays in periodontal disease and to determine the level of IL-11 in HGFs stimulated with IL-1alpha and TNF-alpha.
  
  
  METHODS
  HGFs were stimulated with IL-1alpha and TNF-alpha alone or in combination. The production of IL-11 was measured using enzyme-linked immunosorbent assay (ELISA). IL-11 and Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH) messenger RNA (mRNA) levels in HGFs were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  IL-1alpha significantly increased the levels of IL-11 in HGFs. TNF-alpha also significantly augmented IL-11 production in HGFs, and synergistically stimulated HGFs to produce IL-11 when combined with IL-1alpha. Indomethacin, an inhibitor of prostaglandin synthesis, significantly reduced IL-11 production by HGFs stimulated with IL-1alpha and TNF-alpha individually or in combination. IL-1alpha alone or combined with TNF-alpha enhanced the ratio of IL-11/GAPDH mRNA expression in HGFs, and the augmentation was abolished by indomethacin after co-incubation for 24 hs.
  
  
  CONCLUSIONS
  Production of IL-11 in HGFs stimulated with IL-1alpha and TNF-alpha was transcriptionally upregulated by the endogenous prostaglandin synthesis. Inhibition of prostaglandin might suppress the osteoclastogenesis by IL-11 in inflammatory periodontal diseases.
authors.affiliation: Department of Periodontology, Peking University School of Stomatology, Beijing 100081, China. helu-bj@hotmail.com
authors.forename: Lu
authors.initials: L
authors.lastname: He
authors.forename: T
authors.initials: T
authors.lastname: Nagasawa
authors.forename: I
authors.initials: I
authors.lastname: Ishikawa
mesh_terms: D002478:Cells, Cultured; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism; D005881:Gingiva / Q000166:cytology* / Q000378:metabolism; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D017370:Interleukin-11 / Q000096:biosynthesis*; D053582:Interleukin-1alpha / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D016861:Cyclooxygenase Inhibitors; D017370:Interleukin-11; D053582:Interleukin-1alpha; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007213:Indomethacin