Immune response mediated by Th1 / IL-17 / caspase-9 promotes evolution of periodontal disease

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dc.contributor.authorSommer, M. E. L.
dc.contributor.authorDalia, R. A.
dc.contributor.authorNogueira, A. V. B. [UNESP]
dc.contributor.authorCirelli, J. A. [UNESP]
dc.contributor.authorVinolo, M. A. R.
dc.contributor.authorFachi, J. L.
dc.contributor.authorOliveira, C. A.
dc.contributor.authorAndrade, T. A. M.
dc.contributor.authorMendonca, F. A. S.
dc.contributor.authorSantamaria, M.
dc.contributor.authorFelonato, M.
dc.contributor.institutionCtr Univ Herminio Ometto UNIARARAS
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.date.accessioned2019-10-04T12:32:46Z
dc.date.available2019-10-04T12:32:46Z
dc.date.issued2019-01-01
dc.description.abstractIntroduction: Periodontitis is characterized by inflammatory mediators beyond T lymphocyte function and phenotype (Thl/Th2/Th17). The clinical diversity in periodontitis makes it difficult to characterize the immune response in patients. This study evaluated the profile of the adaptive immune response in the periodontal disease model. Methods: 72 rats (Wistar) were divided into a control group (CTL/day 0) and periodontitis (PD15/15 days and PD60/60 days). In the PD15 and PD60 groups, periodontal disease was induced by ligature with a silk thread placed in the cervical region of the upper first molar. After euthanasia, the periodontal tissue was analyzed by flow cytometry (CD4, CD8, CD25, CD44), semi-quantitative RT-PCR (T-bet, GATA-3, ROR gamma t), semi-quantitative RT-PCR and ELISA IFN-gamma, TNF-alpha, IFN-gamma, IL-4, IL-6, IL-10, IL-17) and by Western blotting (Caspase-9, PCNA). Results: The number of CD4(+) CD25(+), CD4(+) CD44(+), CD8(+) CD25(+) and CD8(+) CD44(+) cells and expression levels of T-bet and GATA-3 are increased in the PD60 group compared to PD15 and CTL. The ROR gamma-t gene transcript increased in the PD15 group in relation to PD60 and CTL. The cytokines IFN-gamma, TNF-alpha and IL-17 increased in the PD60 group in relation to PD15. The expression of Caspase-9 was higher in the PD60 group than in PD15. Conclusions: The results suggest that the evolution of gingivitis to periodontitis is related to the accumulation of activated Thl cells (IFN-gamma and TNF-alpha) associated with the presence of increased IL-17. Studies with inhibitors of these cytokines in periodontal disease may lead to therapy directed at blocking the inflammatory process in this pathology, interrupting bone loss.en
dc.description.affiliationCtr Univ Herminio Ometto UNIARARAS, Grad Program Biomed Sci, Araras, SP, Brazil
dc.description.affiliationCtr Univ Herminio Ometto UNIARARAS, Grad Program Odontol, Araras, SP, Brazil
dc.description.affiliationSao Paulo State Univ, Dept Diag & Surg, Sch Dent, Araraquara, SP, Brazil
dc.description.affiliationUniv Estadual Campinas, Inst Biol, Dept Genet Evolut & Bioagents, Campinas, SP, Brazil
dc.description.affiliationUnespSao Paulo State Univ, Dept Diag & Surg, Sch Dent, Araraquara, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipHerminio Ometto Foundation
dc.description.sponsorshipIdFAPESP: 2012-51110-8
dc.format.extent77-84
dc.identifierhttp://dx.doi.org/10.1016/j.archoralbio.2018.09.009
dc.identifier.citationArchives Of Oral Biology. Oxford: Pergamon-elsevier Science Ltd, v. 97, p. 77-84, 2019.
dc.identifier.doi10.1016/j.archoralbio.2018.09.009
dc.identifier.issn0003-9969
dc.identifier.urihttp://hdl.handle.net/11449/185120
dc.identifier.wosWOS:000451492700011
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofArchives Of Oral Biology
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectCytokines
dc.subjectImmune response
dc.subjectPeriodontitis
dc.subjectLymphocytes
dc.titleImmune response mediated by Th1 / IL-17 / caspase-9 promotes evolution of periodontal diseaseen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.

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