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‐κ B (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). Materials and 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)‐γ, IL‐2, RANK, and RANKL, but not IL‐4. IL‐10 (Th2 cytokine) was detected more frequently in the samples than IFN‐γ 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.