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Clinical associations between IL-17 family cytokines and periodontitis and potential differential roles for IL-17A and IL-17E in periodontal immunity

Lookup NU author(s): Professor Philip Preshaw, Dr John Taylor

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND).


Abstract

IL-17A is implicated in periodontitis pathogenesis. The roles of IL-17B-IL-17F and IL-17A/F are unknown. This study aimed to determine clinical associations between IL-17 family cytokines and periodontitis and to investigate the biological roles of IL-17A and IL-17E using in vitro model systems.Samples from 97 patients with periodontitis and 77 healthy volunteers were used in the study. Serum, saliva and gingival crevicular fluid (GCF) levels of IL-17 family cytokines were measured by ELISA. Oral keratinocytes were stimulated with a P. gingivalis biofilm, or IL-17A, in the presence and absence of IL-17E and the expression of IL-8 and CXCL5 were investigated by ELISA and real-time-PCR. NF-kappa B phosphorylation in similar experiments was also measured using a cell-based ELISA.Serum, saliva and GCF IL-17A levels were higher in periodontitis patients and correlated positively with clinical parameters of attachment loss, pocket depth and bleeding on probing. Serum IL-17E levels were lower in periodontitis patients and the serum IL-17A:IL-17E ratio correlated positively with clinical parameters. In vitro, IL-17E inhibited Porphyromonas gingivalis and IL-17A induced expression of chemokines by reducing phosphorylation of the NF-kappa B p65 subunit.Serum IL-17A:IL-17E may be a marker of disease severity. IL-17E may have opposing roles to IL-17A in periodontitis pathogenesis. IL-17E can negatively regulate IL-17A and periodontal pathogen induced expression of chemokines by oral keratinocytes.


Publication metadata

Author(s): Azman R, Lappin DF, MacPherson A, Riggio M, Robertson D, Hodge P, Ramage G, Culshaw S, Preshaw PM, Taylor J, Nile C

Publication type: Article

Publication status: Published

Journal: Inflammation Research

Year: 2014

Volume: 63

Issue: 12

Pages: 1001-1012

Print publication date: 01/12/2014

Online publication date: 05/11/2014

Acceptance date: 10/10/2014

Date deposited: 30/11/2015

ISSN (print): 1023-3830

ISSN (electronic): 1420-908X

Publisher: Springer

URL: http://dx.doi.org/10.1007/s00011-014-0776-7

DOI: 10.1007/s00011-014-0776-7


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