CCR5 Delta 32 (rs333) polymorphism is associated with decreased risk of chronic and aggressive periodontitis: a case control analysis based in disease resistance and susceptibility phenotypes
Author
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Cavalla Ruiz, Ian Franco
Author
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Biguetti, Claudia C.
Author
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Dionisio, Thiago J.
Author
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Azevedo, Michelle C. S.
Author
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Martins, Walter, Jr.
Author
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Santos, Carlos F.
Author
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Trombone, Ana Paula F.
Author
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Silva, Renato M.
Author
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Letra, Ariadne
Author
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Garlet, Gustavo P.
Admission date
dc.date.accessioned
2018-08-01T16:37:22Z
Available date
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2018-08-01T16:37:22Z
Publication date
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2018
Cita de ítem
dc.identifier.citation
Cytokine, 103 (2018): 142–149
es_ES
Identifier
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10.1016/j.cyto.2017.09.022
Identifier
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https://repositorio.uchile.cl/handle/2250/150529
Abstract
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Chronic and aggressive periodontitis are infectious diseases characterized by the irreversible destruction of periodontal tissues, which is mediated by the host inflammatory immune response triggered by periodontal infection. The chemokine receptor CCR5 play an important role in disease pathogenesis, contributing to pro inflammatory response and osteoclastogenesis. CCR5 Delta 32 (rs333) is a loss-of-function mutation in the CCR5 gene, which can potentially modulate the host response and, consequently periodontitis outcome. Thus, we investigated the effect of the CCR5 Delta 32 mutation over the risk to suffer periodontitis in a cohort of Brazilian patients (total N = 699), representative of disease susceptibility (chronic periodontitis, N = 197; and aggressive periodontitis, N-= 91) or resistance (chronic gingivitis, N = 193) phenotypes, and healthy subjects (N = 218). Additionally, we assayed the influence of CCR5 Delta 32 in the expression of the biomarkers TNFa, IL-10, IL-6, IFN-y and T-bet, and key periodontal pathogens P. gingivalis, T. forsythia, and T. denticola. In the association analysis of resistant versus susceptible subjects, CCR5 Delta 32 mutant allele-carriers proved significantly protected against chronic (OR 0.49; 95% CI 0.29-0.83; p-value 0.01) and aggressive (OR 0.46; 95% CI 0.22-0.94; p-value 0.03) periodontitis. Further, heterozygous subjects exhibited significantly decreased expression of TNFa in periodontal tissues, pointing to a functional effect of the mutation in periodontal tissues during the progression of the disease. Conversely, no significant changes were observed in the presence or quantity of the periodontal pathogens P. gingivalis, T. forsythia, and T. denticola in the subgingival biofilm that could be attributable to the mutant genotype.
es_ES
Patrocinador
dc.description.sponsorship
Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
2014/03276-0
2014/17886-4
CCR5 Delta 32 (rs333) polymorphism is associated with decreased risk of chronic and aggressive periodontitis: a case control analysis based in disease resistance and susceptibility phenotypes