Salivary IL17 and IL35 Suppresses Cell Progression in Periodontal Disease Manipulation Induced by TNBs via NF-κB Signaling Pathway IL17 and IL35 in periodontal disease and systemic osteoporosis

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Yunxiao Wang
Ling Wang


Periodontal disease, IL17, IL35, chronic periodontitis (CP), inflammatory markers, NF-κB


Background: Periodontal disease prognosis relies primarily on clinical and radiographic parameters. In present study association of interleukins IL17 & IL35 levels in GCF and serum among healthy, gingivitis, and chronic periodontitis (CP) individuals is examined and possibility of using them as possible prognosis marker for periodontal disease activity is explored. Expressions of TNF-α, AKT and NF-κB. Inflammatory cells were evaluated in both cases. Methods: This prospective study was accomplished on patients with osteoporosis and a comprehensive periodontal examination was performed including standardized digital dental periapical radiographs and bone mineral density (BMD) evaluation. ELISA kit was used for quantifying levels of IL-17 and IL-35 in the patients’ plasma. ELISA was used to check expressions level of TNF-α, and NF-κB. Inflammatory cells in both cases. STATA15.0 was used for statistical analysis and a p value ≤0.05 was considered statistically significant. Results: The mean of GI of healthy and osteoporotic group were much lower than periodontitis group.  PI, PPD and CAL were almost comparable between healthy control group and osteoporotic group. Plasma IP-17 level and IL35 level where raised in periodontitis group compare to health control and also were significant different from osteoporosis groups. Although IL17 value of osteoporosis group was comparable to health group, IL 35 had significant high value than healthy. Expressions of TNF-α were increased in periodontitis group. Expressions of phosphorylated PI3K and AKT were reduced in periodontitis group. Meanwhile, expressions of NF-κB were decreased periodontitis group compared to systemic osteoporosis. Conclusion: Various studies characterized the host response to infection in periodontal/periapical diseases, they are found to be very different from those of systemic osetoporesis, however this is first to study IL17 and Il35 in such cases. Periodontitis inhibits inflammatory cell process and regulates related factors during pathogenesis, suggesting that through PI3K/AKT/NF-κB signaling pathway disease progression in periodontitis are modulated.

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1. Pihlstrom BL, Michalowicz BS, Johnson NW. Periodontal diseases. The lancet. 2005; 366(9499):1809-20.
2. Cekici A, Kantarci A, Hasturk H, Van Dyke TE. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontology 2000. 2014; 64(1):57-80.
3. Lockhart PB, Bolger AF, Papapanou PN, Osinbowale O, Trevisan M, Levison ME, Taubert KA, Newburger JW, Gornik HL, Gewitz MH, Wilson WR. Periodontal disease and atherosclerotic vascular disease: does the evidence support an independent association? A scientific statement from the American Heart Association. Circulation. 2012; 125(20):2520-44.
4. Stabholz A, Soskolne WA, Shapira L. Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis. Periodontology. 2010; 53(1):138-53.
5. Weaver CT, Hatton RD, Mangan PR, Harrington LE. IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu. Rev. Immunol. 2007; 25:821-52.
6. Sakkas LI, Mavropoulos A, Perricone C, Bogdanos DP. IL-35: a new immunomodulator in autoimmune rheumatic diseases. Immunologic research. 2018:1-8.
7. Saito S, Nakashima A, Ito M, Shima T. Clinical implication of recent advances in our understanding of IL-17 and reproductive immunology. Expert review of clinical immunology. 20117(5):649-57.
8. Garcia RI, Henshaw MM, Krall EA. Relationship between periodontal disease and systemic health. Periodontology. 2001 Feb; 25(1):21-36.
9. Hahn CL, Liewehr FR. Innate immune responses of the dental pulp to caries. Journal of endodontics. 2007; 33(6):643-51.
10. DeSelm CJ, Takahata Y, Warren J, Chappel JC, Khan T, Li X, Liu C, Choi Y, Kim YF, Zou W, Teitelbaum SL. IL‐17 mediates estrogen‐deficient osteoporosis in an Act1‐dependent manner. Journal of cellular biochemistry. 2012; 113(9):2895-902.
11. Miossec P, Korn T, Kuchroo VK. Interleukin-17 and type 17 helper T cells. New England Journal of Medicine. 2009; 361(9):888-98.
12. Martinez GJ, Nurieva RI, Yang XO, Dong C. Regulation and function of proinflammatory TH17 cells. Annals of the New York Academy of Sciences. 2008; 1143(1):188-211.
13. Goswami J, Hernández‐Santos N, Zuniga LA, Gaffen SL. A bone‐protective role for IL‐17 receptor signaling in ovariectomy‐induced bone loss. European journal of immunology. 2009; 39(10):2831-9.
14. Ivanov II, McKenzie BS, Zhou L, Tadokoro CE, Lepelley A, Lafaille JJ, Cua DJ, Littman DR. The orphan nuclear receptor RORγt directs the differentiation program of proinflammatory IL-17+ T helper cells. Cell. 2006; 126(6):1121-33.
15. Sato K, Suematsu A, Okamoto K, Yamaguchi A, Morishita Y, Kadono Y, Tanaka S, Kodama T, Akira S, Iwakura Y, Cua DJ. Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction. Journal of Experimental Medicine. 2006; 203(12):2673-82.
16. Veldhoen M, Hocking RJ, Atkins CJ, Locksley RM, Stockinger B. TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Immunity. 2006; 24(2):179-89.
17. Tanaka, T., M. Narazaki, and T. Kishimoto, IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol, 2014. 6(10): p. a016295.
18. Xiao, Y.T., et al., Neutralization of IL-6 and TNF-alpha ameliorates intestinal permeability in DSS-induced colitis. Cytokine, 2016. 83: p. 189-192.
19. Lopetuso, L.R., et al., Harmful Effects and Potential Benefits of Anti-Tumor Necrosis Factor (TNF)-alpha on the Liver. Int J Mol Sci, 2018. 19(8).
20. Wymann, M.P. and L. Pirola, Structure and function of phosphoinositide 3-kinases. Biochim Biophys Acta, 1998. 1436(1-2): p. 127-5
21. Sui, L., J. Wang, and B.M. Li, Role of the phosphoinositide 3-kinase-Akt-mammalian target of the rapamycin signaling pathway in long-term potentiation and trace fear conditioning memory in rat medial prefrontal cortex. Learn Mem, 2008. 15(10): 762-76.
22. Hozumi, H., et al., Endoscopic finding of spontaneous hemorrhage correlates with tumor necrosis factor alpha expression in colonic mucosa of patients with ulcerative colitis. Int J Colorectal Dis, 2013. 28(8): 1049-55.