title: The potential role of interleukin-17 in the immunopathology of periodontal disease.
abstract: BACKGROUND
  Interleukin-17 (IL-17) is exclusively produced by activated T cells, and this cytokine can induce inflammatory responses, support immune responses (Th1), and stimulate osteoclastic bone resorption in combination with receptor activator of NF-kappaB (RANK) and RANK ligand (RANKL). These biological functions are relevant to the aetiopathogenesis of periodontitis, and thus we sought to investigate whether IL-17 is produced in periodontal lesions and to assess the relationship of gene expression between IL-17 and other cytokines, and to determine the effect of IL-17 on IL-6 production in human gingival fibroblasts (HGF).
  
  
  METHODS
  IL-17 was detected and measured in periodontal tissues obtained as biopsy samples during periodontal surgery and in the cell-free culture supernatants cultured ex vivo, by using Western immunoblotting and enzyme-linked immunosorbent assay, respectively. IL-17 and other cytokine gene expression were investigated by the reverse transcription-polymerase chain reaction (RT-PCR) method. The contribution of IL-17 to IL-6 production by HGF was studied.
  
  
  RESULTS
  IL-17 protein was moderately detected in periodontal tissues. In contrast, IL-17 mRNA was expressed only in nine of 23 periodontitis tissue samples by RT-PCR. The IL-17 mRNA-positive samples simultaneously expressed mRNAs encoding interferon (IFN)-gamma, IL-2, RANK, and RANKL, but not IL-4. IL-10 (Th2 cytokine) was detected more frequently in the samples than IFN-gamma and IL-2 (Th1 cytokine). Recombinant human IL-17 induced IL-6 production from HGF in a dose- and time-dependent fashion.
  
  
  CONCLUSIONS
  These results indicate that IL-17 is produced in periodontal lesions, which may be involved in Th1 modulation and enhance inflammatory reactions via gingival fibroblast-derived mediators in periodontal disease. Thus, IL-17, together with other cytokines, has a potential role in the aetiopathogenesis of periodontal disease.
authors.affiliation: Department of Endodontics, Meikai University School of Dentistry, Saitama, Japan.
authors.forename: Keiso
authors.initials: K
authors.lastname: Takahashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Azuma
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Motohira
authors.forename: D F
authors.initials: DF
authors.lastname: Kinane
authors.forename: Shin
authors.initials: S
authors.lastname: Kitetsu
mesh_terms: D000328:Adult; D000368:Aged; D002352:Carrier Proteins / Q000096:biosynthesis; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D005881:Gingiva / Q000166:cytology / Q000378:metabolism; D006801:Humans; D020381:Interleukin-17 / Q000096:biosynthesis* / Q000502:physiology*; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D008875:Middle Aged; D010518:Periodontitis / Q000276:immunology* / Q000378:metabolism; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000378:metabolism; D046509:Tissue Culture Techniques
chemical_list: D002352:Carrier Proteins; D016207:Cytokines; D020381:Interleukin-17; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505686:TNFRSF11A protein, human; C505688:TNFSF11 protein, human