BACKGROUND: Growing evidence suggests that individual genetic susceptibility may influence the host's response to infections. Previously, we showed that a common variation in the interleukin (IL)-6 gene was associated with increased odds of detection of common periodontal pathogens from individuals with aggressive periodontitis. The aim of this study was to investigate the association between IL-6 polymorphisms and periodontopathogenic bacteria in a larger, ethnically mixed population of subjects with periodontitis. METHODS: Genomic DNA was extracted from 107 subjects diagnosed with severe forms of periodontitis to study a cluster of polymorphisms in inflammatory genes, including IL-6. The presence of Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, and Tannerella forsythia (previously T. forsythensis) in their subgingival biofilm was determined by polymerase chain reaction analysis. Serum IL-6 and C-reactive protein (CRP) concentrations were analyzed by enzyme-linked immunosorbent assay. RESULTS: Multiple logistic regression analysis revealed that the IL-6 -6106 polymorphism was associated with the detection of A. actinomycetemcomitans (P = 0.009; odds ratio [OR] = 3.5; 95% confidence interval [CI]: 1.38 to 9.16) and the concomitant detection of A. actinomycetemcomitans and P. gingivalis (P = 0.015; OR = 3.6; 95% CI: 1.28 to 10.04). The IL-6 -174 polymorphism was associated with increased odds of the concomitant detection of A. actinomycetemcomitans and P. gingivalis (P = 0.042; OR = 2.8; 95% CI: 1.04 to 7.75). Haplotype analysis of all five IL-6 polymorphisms confirmed an association with the detection of A. actinomycetemcomitans (P = 0.046). The IL-6 -6106 polymorphism was also associated with CRP serum levels at multivariate analysis (P = 0.024). CONCLUSIONS: These findings confirm the hypothesis that complex interactions between the microbiota and host genome are at the basis of susceptibility to periodontitis. Periodontal disease may represent a useful model to study the pathways and mechanisms of host-pathogen interactions in inflammatory diseases.
BACKGROUND: Growing evidence suggests that individual genetic susceptibility may influence the host's response to infections. Previously, we showed that a common variation in the interleukin (IL)-6 gene was associated with increased odds of detection of common periodontal pathogens from individuals with aggressive periodontitis. The aim of this study was to investigate the association between IL-6 polymorphisms and periodontopathogenic bacteria in a larger, ethnically mixed population of subjects with periodontitis. METHODS: Genomic DNA was extracted from 107 subjects diagnosed with severe forms of periodontitis to study a cluster of polymorphisms in inflammatory genes, including IL-6. The presence of Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, and Tannerella forsythia (previously T. forsythensis) in their subgingival biofilm was determined by polymerase chain reaction analysis. Serum IL-6 and C-reactive protein (CRP) concentrations were analyzed by enzyme-linked immunosorbent assay. RESULTS: Multiple logistic regression analysis revealed that the IL-6 -6106 polymorphism was associated with the detection of A. actinomycetemcomitans (P = 0.009; odds ratio [OR] = 3.5; 95% confidence interval [CI]: 1.38 to 9.16) and the concomitant detection of A. actinomycetemcomitans and P. gingivalis (P = 0.015; OR = 3.6; 95% CI: 1.28 to 10.04). The IL-6 -174 polymorphism was associated with increased odds of the concomitant detection of A. actinomycetemcomitans and P. gingivalis (P = 0.042; OR = 2.8; 95% CI: 1.04 to 7.75). Haplotype analysis of all five IL-6 polymorphisms confirmed an association with the detection of A. actinomycetemcomitans (P = 0.046). The IL-6 -6106 polymorphism was also associated with CRP serum levels at multivariate analysis (P = 0.024). CONCLUSIONS: These findings confirm the hypothesis that complex interactions between the microbiota and host genome are at the basis of susceptibility to periodontitis. Periodontal disease may represent a useful model to study the pathways and mechanisms of host-pathogen interactions in inflammatory diseases.
Authors: L S Finoti; S C T Corbi; G Anovazzi; S R L Teixeira; J P Steffens; R Secolin; Y J Kim; S R P Orrico; J A Cirelli; M P A Mayer; R M Scarel-Caminaga Journal: Eur J Clin Microbiol Infect Dis Date: 2013-05-10 Impact factor: 3.267
Authors: L S Finoti; G Anovazzi; S C Pigossi; S C T Corbi; S R L Teixeira; G V V Braido; Y J Kim; S R P Orrico; J A Cirelli; M P A Mayer; R M Scarel-Caminaga Journal: Eur J Clin Microbiol Infect Dis Date: 2013-06-08 Impact factor: 3.267
Authors: Adrien Boillot; Ryan T Demmer; Ziad Mallat; Ralph L Sacco; David R Jacobs; Joelle Benessiano; Alain Tedgui; Tatjana Rundek; Panos N Papapanou; Moïse Desvarieux Journal: Atherosclerosis Date: 2015-07-22 Impact factor: 5.162
Authors: L Nibali; G Pelekos; F D'Aiuto; N Chaudhary; R Habeeb; D Ready; M Parkar; N Donos Journal: Clin Oral Investig Date: 2012-08-24 Impact factor: 3.573
Authors: Samuel B Ferreira; Ana Paula F Trombone; Carlos E Repeke; Cristina R Cardoso; Walter Martins; Carlos F Santos; Paula Cristina Trevilatto; Mario J Avila-Campos; Ana Paula Campanelli; João S Silva; Gustavo P Garlet Journal: Infect Immun Date: 2008-06-09 Impact factor: 3.441
Authors: A V Safonova; A N Petrin; S D Arutyunov; V N Tsarev; L A Akulenko; A O Zorina; D V Rebrikov; A V Rubanovich; S A Borinskaya; N K Yankovsky Journal: Acta Naturae Date: 2011-01 Impact factor: 1.845