Overexpression and Potential Regulatory Role of IL-17F in Pathogenesis of Chronic Periodontitis
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The objective of this study was to investigate the expression level, clinical significance, and possible regulating role of IL-17F in patients of chronic periodontitis. Periodontal local tissues were obtained from chronic periodontitis (CP) and healthy controls (HC) for real-time PCR (RT-PCR) detection with IL-17F and IL-17A messenger RNA (mRNA). Primary human gingival fibroblasts (HGF) were derived from patients receiving crown-lengthening procedures. Efficiency of small interfering RNA (siRNA) of IL-17R to HGF cells were assessed by Western blot and RT-PCR. Recombinant IL-17F and IL-17A were used to stimulate the HGF cells compared with the control group. Aspects of the nuclear factor-kappa B (NF-κB) and extracellular signal-regulated kinase (ERK) signaling pathways were examined by Western blot. Production of pro-inflammatory cytokines induced by IL-17F and IL-17A was detected by RT-PCR. Statistical analysis was analyzed by SPSS software. It showed significantly elevated levels of IL-17F and IL-17A mRNA in CP gingival tissues compared with HC group (P < 0.01). Further analysis showed a significant correlation between IL-17F and IL-17A mRNA in CP group (P < 0.05), and both cytokines also correlated with the probing depth (P < 0.05). Recombinant IL-17F can induce NF-κB phosphor-p65 and ERK phosphorylation of HGF cells similar to that of IL-17A. Interestingly, we found that both IL-17F and IL-17A could promote the important inflammatory cytokines IL-6, CXCL8, and CCL20 production compared with IL-17R siRNA group (P < 0.05). This study indicates that IL-17F may be involved in pathogenesis of periodontitis like IL-17A. The role of IL-17F in disease pathogenesis needs to be further investigated.
KEY WORDSperiodontitis interleukin-17F (IL-17F) interleukin-17A (IL-17A)
This work was supported by grants from the National Natural Science Foundation of China (81371150, 81400517), China Postdoctoral Science Foundation funded project (No. 2014M550767), and Project supported by Beijing Postdoctoral Research Foundation (2014ZZ-02).
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