Sequential IL-23 and IL-17 and increased Mmp8 and Mmp14 expression characterize the progression of an experimental model of periodontal disease in type 1 diabetes

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dc.contributor.authorSilva, Juliete A. F.
dc.contributor.authorFerrucci, Danilo L.
dc.contributor.authorPeroni, Luis A.
dc.contributor.authorAbrahao, Patricia G. S.
dc.contributor.authorSalamene, Aline F.
dc.contributor.authorRossa-Junior, Carlos [UNESP]
dc.contributor.authorCarvalho, Hernandes F.
dc.contributor.authorStach-Machado, Dagmar R.
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionNatl Inst Sci & Technol Photon Appl Cell Biol INF
dc.date.accessioned2013-09-30T18:31:52Z
dc.date.accessioned2014-05-20T13:45:26Z
dc.date.available2013-09-30T18:31:52Z
dc.date.available2014-05-20T13:45:26Z
dc.date.issued2012-06-01
dc.description.abstractMolecular mechanisms responsible for periodontal disease (PD) and its worsening in type 1 Diabetes Mellitus (DM1) remain unknown. Cytokine profile and expression levels of collagenases, Mmp14, and tissue inhibitors were determined, as were the numbers of neutrophils and macrophages in combined streptozotocin-induced DM1 and ligature-induced PD models. Increased IL-23 (80-fold) and Mmp8 expression (25-fold) was found in DM1. Ligature resulted in an IL-1 beta/IL-6 profile, increased expression of Mmp8, Mmp13, and Mmp14 (but not Mmp1), and transient expression of Timp1 and Reck in non-diabetics. PD in DM1 involved IL-1 beta (but not IL-6) and IL-23/IL-17, reduced IL-6 and IL-10, sustained Mmp8 and Mmp14, increased Mmp13 and reduced Reck expression in association with 20-fold higher counts of neutrophils and macrophages. IL-23 and Mmp8 expression are hallmarks of DM1. In association with the IL-1/IL-6 (Th1) response in PD, one found a secondary IL-17 (Th17) pathway in non-diabetic rats. Low IL-6/TNF-a suggest that the Th1 response was compromised in DM1, while IL-17 indicates a prevalence of the Th17 pathway, resulting in high neutrophil recruitment. Mmp8, Mmp13, and Mmp14 expression seems important in the tissue destruction during PD in DM1. PD-associated IL-1/IL-6 (Th1), IL-10, and Reck expression are associated with the acute-to-chronic inflammation transition, which is lost in DM1. In conclusion, IL-23/IL-17 are associated with the PD progression in DM1. J. Cell. Physiol. 227: 24412450, 2012. (c) 2011 Wiley Periodicals, Inc.en
dc.description.affiliationState Univ Campinas UNICAMP, Dept Anat Cell Biol Physiol & Biophys, Campinas, SP, Brazil
dc.description.affiliationAraraquara UNESP, Sch Dent, Dept Diag & Surg, São Paulo, Brazil
dc.description.affiliationNatl Inst Sci & Technol Photon Appl Cell Biol INF, Campinas, SP, Brazil
dc.description.affiliationUnespAraraquara UNESP, Sch Dent, Dept Diag & Surg, São Paulo, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipIdFAPESP: 08/54958-2
dc.description.sponsorshipIdFAPESP: 09/016150-6
dc.description.sponsorshipIdCNPq: 479074/08-9
dc.format.extent2441-2450
dc.identifierhttp://dx.doi.org/10.1002/jcp.22979
dc.identifier.citationJournal of Cellular Physiology. Malden: Wiley-blackwell, v. 227, n. 6, p. 2441-2450, 2012.
dc.identifier.doi10.1002/jcp.22979
dc.identifier.issn0021-9541
dc.identifier.urihttp://hdl.handle.net/11449/15983
dc.identifier.wosWOS:000300719600017
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofJournal of Cellular Physiology
dc.relation.ispartofjcr3.923
dc.relation.ispartofsjr1,641
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.titleSequential IL-23 and IL-17 and increased Mmp8 and Mmp14 expression characterize the progression of an experimental model of periodontal disease in type 1 diabetesen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderWiley-blackwell
unesp.author.lattes7634063102292261[6]
unesp.author.orcid0000-0002-7568-2275[2]
unesp.author.orcid0000-0003-1705-5481[6]
unesp.author.orcid0000-0002-4543-5169[1]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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