Publicação:
Green tea extract and its major constituent, epigallocatechin-3-gallate, induce epithelial beta-defensin secretion and prevent beta-defensin degradation by Porphyromonas gingivalis

dc.contributor.authorLombardo Bedran, T. B. [UNESP]
dc.contributor.authorFeghali, K.
dc.contributor.authorZhao, L.
dc.contributor.authorPalomari Spolidorio, D. M. [UNESP]
dc.contributor.authorGrenier, D.
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniv Laval
dc.contributor.institutionSichuan Univ
dc.date.accessioned2015-03-18T15:55:20Z
dc.date.available2015-03-18T15:55:20Z
dc.date.issued2014-10-01
dc.description.abstractBackground and Objective: Antimicrobial peptides, such as beta-defensins, secreted by gingival epithelial cells, are thought to play a major role in preventing periodontal diseases. In the present study, we investigated the ability of green tea polyphenols to induce human beta-defensin (hBD) secretion in gingival epithelial cells and to protect hBDs from proteolytic degradation by Porphyromonas gingivalis.Material and Methods: Gingival epithelial cells were treated with various amounts (25-200 mu g/mL) of green tea extract or epigallocatechin-3-gallate (EGCG). The secretion of hBD1 and hBD2 was measured using ELISAs, and gene expression was quantified by real-time PCR. The treatments were also carried out in the presence of specific kinase inhibitors to identify the signaling pathways involved in hBD secretion. The ability of green tea extract and EGCG to prevent hBD degradation by proteases of P. gingivalis present in a bacterial culture supernatant was evaluated by ELISA.Results: The secretion of hBD1 and hBD2 was up-regulated, in a dose-dependent manner, following the stimulation of gingival epithelial cells with a green tea extract or EGCG. Expression of the hBD gene in gingival epithelial cells treated with green tea polyphenols was also increased. EGCG-induced secretion of hBD1 and hBD2 appeared to involve extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase. Lastly, green tea extract and EGCG prevented the degradation of recombinant hBD1 and hBD2 by a culture supernatant of P. gingivalis.Conclusion: Green tea extract and EGCG, through their ability to induce hBD secretion by epithelial cells and to protect hBDs from proteolytic degradation by P. gingivalis, have the potential to strengthen the epithelial antimicrobial barrier. Future clinical studies will indicate whether these polyphenols represent a valuable therapeutic agent for treating/preventing periodontal diseases.en
dc.description.affiliationState Univ Sao Paulo, Araraquara Dent Sch, Dept Oral Diag & Surg, Araraquara, SP, Brazil
dc.description.affiliationUniv Laval, Fac Dent, Oral Ecol Res Grp, Quebec City, PQ G1V 0A6, Canada
dc.description.affiliationSichuan Univ, West China Hosp Stomatol, Dept Periodont, Chengdu 610064, Sichuan, Peoples R China
dc.description.affiliationUnespState Univ Sao Paulo, Araraquara Dent Sch, Dept Oral Diag & Surg, Araraquara, SP, Brazil
dc.description.sponsorshipCanadian Institutes of Health Research
dc.format.extent615-623
dc.identifierhttp://dx.doi.org/10.1111/jre.12142
dc.identifier.citationJournal Of Periodontal Research. Hoboken: Wiley-blackwell, v. 49, n. 5, p. 615-623, 2014.
dc.identifier.doi10.1111/jre.12142
dc.identifier.issn0022-3484
dc.identifier.urihttp://hdl.handle.net/11449/117146
dc.identifier.wosWOS:000341884200009
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofJournal Of Periodontal Research
dc.relation.ispartofjcr2.878
dc.relation.ispartofsjr0,927
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectbeta-defensinen
dc.subjectepigallocatechin gallateen
dc.subjectepithelial cellsen
dc.subjectgreen teaen
dc.subjectperiodontal diseaseen
dc.subjectPorphyromonas gingivalisen
dc.titleGreen tea extract and its major constituent, epigallocatechin-3-gallate, induce epithelial beta-defensin secretion and prevent beta-defensin degradation by Porphyromonas gingivalisen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderWiley-Blackwell
dspace.entity.typePublication
unesp.author.orcid0000-0003-2376-1024[4]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentDiagnóstico e Cirurgia - FOARpt

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