Skip to main content

Advertisement

Log in

Overexpression and Potential Regulatory Role of IL-17F in Pathogenesis of Chronic Periodontitis

  • Published:
Inflammation Aims and scope Submit manuscript

Abstract

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.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2
Fig. 3
Fig. 4
Fig. 5

Similar content being viewed by others

REFERENCES

  1. Beklen, A., M. Ainola, M. Hukkanen, C. Gurgan, T. Sorsa, and Y.T. Konttinen. 2007. MMPs, IL-1, and TNF are regulated by IL-17 in periodontitis. Journal of Dental Research 86(4): 347–351.

    Article  CAS  PubMed  Google Scholar 

  2. Tesmer, L.A., S.K. Lundy, S. Sarkar, and D.A. Fox. 2008. Th17 cells in human disease. Immunology Reviews 223: 87–113.

    Article  CAS  Google Scholar 

  3. Zhao, L., Y. Zhou, Y. Xu, Y. Sun, L. Li, and W. Chen. 2011. Effect of non-surgical periodontal therapy on the levels of Th17/Th1/Th2 cytokines and their transcription factors in Chinese chronic periodontitis patients. Journal of Clinical Periodontology 38(6): 509–516.

    Article  CAS  PubMed  Google Scholar 

  4. Cardoso, C.R., G.P. Garlet, G.E. Crippa, et al. 2009. Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease. Oral Microbiology and Immunology 24(1): 1–6.

    Article  CAS  PubMed  Google Scholar 

  5. Wang, H., Q. Han, Z. Luo, et al. 2014. Oral lichen planus may enhance the expression of Th17-associated cytokines inlocal lesions of chronic periodontitis. Clinical Oral Investigations 18(6): 1647–1654.

    Article  PubMed  Google Scholar 

  6. Wang, H., Z. Luo, L. Lei, et al. 2013. Interaction between oral lichen planus and chronic periodontitis with Th17-associated cytokines in serum. Inflammation 36(3): 696–704.

    Article  CAS  PubMed  Google Scholar 

  7. Gaffen, S.L., and G. Hajishengallis. 2008. A new inflammatory cytokine on the block: re-thinking periodontal disease and the Th1/Th2 paradigm in the context of Th17 cells and IL-17. Journal of Dental Research 87(9): 817–828.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  8. Yu, J.J., M.J. Ruddy, G.C. Wong, et al. 2007. An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor-dependent signals. Blood 109(9): 3794–3802.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  9. Lu R, Zeng X, AO, et al. 2014. Overexpression and selectively regulatory roles of IL-23/IL-17 axis in the lesions of oral lichen planus. Mediators of Inflammation 2014: 701094.

  10. Chang, S.H., and C. Dong. 2009. IL-17F: regulation, signaling and function in inflammation. Cytokine 46(1): 7–11.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  11. Dong, C. 2009. Differentiation and function of pro-inflammatory Th17 cells. Microbes and Infection 11(5): 584–588.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  12. Chang, S.H., and C. Dong. 2007. A novel heterodimeric cytokine consisting of IL-17 and IL-17F regulates inflammatory responses. Cell Research 17(5): 435–440.

    PubMed  Google Scholar 

  13. Correa, J.D., M.F. Madeira, R.G. Resende, et al. 2012. Association between polymorphisms in interleukin-17A and -17F genes and chronic periodontal disease. Mediators of Inflammation 2012: 846052.

    Article  PubMed Central  PubMed  Google Scholar 

  14. Sun, H., and S. Li. 2012. [Expression of interleukin-17F in human apical periodontitis lesions]. Zhonghua Kou Qiang Yi Xue Za Zhi 47(6): 345–349.

    CAS  PubMed  Google Scholar 

  15. Mahanonda, R., and S. Pichyangkul. 2007. Toll-like receptors and their role in periodontal health and disease. Periodontology 2000 43: 41–55.

    Article  PubMed  Google Scholar 

  16. Baek, K.J., Y. Choi, and S. Ji. 2013. Gingival fibroblasts from periodontitis patients exhibit inflammatory characteristics in vitro. Archives of Oral Biology 58(10): 1282–1292.

    Article  CAS  PubMed  Google Scholar 

  17. Kong, L., X. Qi, S. Huang, S. Chen, Y. Wu, and L. Zhao. 2014. Theaflavins inhibits pathogenic properties of P. gingivalis and MMPs production in P. gingivalis-stimulated human gingival fibroblasts. Archives of Oral Biology 60(1): 12–22.

    Article  PubMed  Google Scholar 

  18. Guo, S., W. Guo, Y. Ding, et al. 2013. Comparative study of human dental follicle cell sheets and periodontal ligament cell sheets for periodontal tissue regeneration. Cell Transplantation 22(6): 1061–1073.

    Article  PubMed  Google Scholar 

  19. McGeachy, M.J., and D.J. Cua. 2008. Th17 cell differentiation: the long and winding road. Immunity 28(4): 445–453.

    Article  CAS  PubMed  Google Scholar 

  20. Conti, H.R., F. Shen, N. Nayyar, et al. 2009. Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis. Journal of Experimental Medicine 206(2): 299–311.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  21. Marks, B.R., and J. Craft. 2009. Barrier immunity and IL-17. Seminars in Immunology 21(3): 164–171.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  22. Gaffen, S.L., J.M. Kramer, J.J. Yu, and F. Shen. 2006. The IL-17 cytokine family. Vitamins and Hormones 74: 255–282.

    Article  CAS  PubMed  Google Scholar 

  23. Lubberts, E. 2010. Th17 cytokines and arthritis. Seminars in Immunopathology 32(1): 43–53.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  24. van Hamburg, J.P., P.S. Asmawidjaja, N. Davelaar, et al. 2011. Th17 cells, but not Th1 cells, from patients with early rheumatoid arthritis are potent inducers of matrix metalloproteinases and proinflammatory cytokines upon synovial fibroblast interaction, including autocrine interleukin-17A production. Arthritis and Rheumatism 63(1): 73–83.

    Article  PubMed  Google Scholar 

  25. Kolls, J.K., and A. Linden. 2004. Interleukin-17 family members and inflammation. Immunity 21(4): 467–476.

    Article  CAS  PubMed  Google Scholar 

  26. Iwakura, Y., H. Ishigame, S. Saijo, and S. Nakae. 2011. Functional specialization of interleukin-17 family members. Immunity 34(2): 149–162.

    Article  CAS  PubMed  Google Scholar 

  27. Yang, X.O., S.H. Chang, H. Park, et al. 2008. Regulation of inflammatory responses by IL-17F. Journal of Experimental Medicine 205(5): 1063–1075.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  28. Noh, M.K., M. Jung, S.H. Kim, et al. 2013. Assessment of IL-6, IL-8 and TNF-alpha levels in the gingival tissue of patients with periodontitis. Experimental and Therapeutic Medicine 6(3): 847–851.

    PubMed Central  CAS  PubMed  Google Scholar 

  29. Mucida, D., and S. Salek-Ardakani. 2009. Regulation of TH17 cells in the mucosal surfaces. Journal of Allergy and Clinical Immunology 123(5): 997–1003.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  30. Luo, Z., H. Wang, Z. Sun, W. Luo, and Y. Wu. 2013. Expression of IL-22, IL-22R and IL-23 in the peri-implant soft tissues of patients with peri-implantitis. Archives of Oral Biology 58(5): 523–529.

    Article  CAS  PubMed  Google Scholar 

  31. Moutsopoulos, N.M., H.M. Kling, N. Angelov, et al. 2012. Porphyromonas gingivalis promotes Th17 inducing pathways in chronic periodontitis. Journal of Autoimmunity 39(4): 294–303.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  32. Vernal, R., N. Dutzan, A. Chaparro, J. Puente, V.M. Antonieta, and J. Gamonal. 2005. Levels of interleukin-17 in gingival crevicular fluid and in supernatants of cellular cultures of gingival tissue from patients with chronic periodontitis. Journal of Clinical Periodontology 32(4): 383–389.

    Article  PubMed  Google Scholar 

  33. Hosokawa, Y., I. Hosokawa, K. Ozaki, H. Nakae, and T. Matsuo. 2012. Interleukin (IL)-17A synergistically enhances CC chemokine ligand 20 production in IL-1beta-stimulated human gingival fibroblasts. Human Immunology 73(1): 26–30.

    Article  CAS  PubMed  Google Scholar 

  34. Hosokawa, Y., I. Hosokawa, K. Ozaki, T. Nakanishi, H. Nakae, and T. Matsuo. 2009. Catechins inhibit CCL20 production in IL-17A-stimulated human gingival fibroblasts. Cellular Physiology and Biochemistry 24(5–6): 391–396.

    Article  CAS  PubMed  Google Scholar 

Download references

ACKNOWLEDGMENTS

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).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Hui Wang.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Luo, Z., Wang, H., Chen, J. et al. Overexpression and Potential Regulatory Role of IL-17F in Pathogenesis of Chronic Periodontitis. Inflammation 38, 978–986 (2015). https://doi.org/10.1007/s10753-014-0060-6

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10753-014-0060-6

KEY WORDS

Navigation