Toll-like receptor 2 knockdown modulates interleukin (IL)-6 and IL-8 but not stromal derived factor-1 (SDF-1/CXCL12) in human periodontal ligament and gingival fibroblasts

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dc.contributor.authorMorandini, Ana Carolina F.
dc.contributor.authorSouza, Pedro Paulo Chaves [UNESP]
dc.contributor.authorRamos-Junior, Erivan Schnaider
dc.contributor.authorBrozoski, Daniel Thomas
dc.contributor.authorSipert, Carla Renata
dc.contributor.authorSouza Costa, Carlos Alberto [UNESP]
dc.contributor.authorSantos, Carlos Ferreira
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionFederal University of Rio de Janeiro
dc.date.accessioned2014-05-27T11:28:48Z
dc.date.available2014-05-27T11:28:48Z
dc.date.issued2013-04-01
dc.description.abstractBackground: Fibroblasts are now seen as active components of the immune response because these cells express Toll-like receptors (TLRs), recognize pathogen-associated molecular patterns, and mediate the production of cytokines and chemokines during inflammation. The innate host response to lipopolysaccharide (LPS) from Porphyromonas gingivalis is unusual inasmuch as different studies have reported that it can be an agonist for Toll-like receptor 2 (TLR2) and an antagonist or agonist for Toll-like receptor 4 (TLR4). This study investigates and compares whether signaling through TLR2 or TLR4 could affect the secretion of interleukin (IL)-6, IL-8, and stromal derived factor-1 (SDF-1/CXCL12) in both human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPDLF). Methods: After small interfering RNA-mediated silencing of TLR2 and TLR4, HGF and HPDLF from the same donors were stimulated with P. gingivalis LPS or with two synthetic ligands of TLR2, Pam2CSK4 and Pam3CSK4, for 6 hours. IL-6, IL-8, and CXCL12mRNA expression and protein secretion were evaluated by quantitative polymerase chain reaction and enzymelinked immunosorbent assay, respectively. Results: TLR2 mRNA expression was upregulated in HGF but not in HPDLF by all the stimuli applied. Knockdown of TLR2 decreased IL-6 and IL-8 in response to P. gingivalis LPS, or Pam2CSK4 and Pam3CSK4, in a similar manner in both fibroblasts subpopulations. Conversely, CXCL12 remained unchanged by TLR2 or TLR4 silencing. Conclusion: These results suggest that signaling through TLR2 by gingival and periodontal ligament fibroblasts can control the secretion of IL-6 and IL-8, which contribute to periodontal pathogenesis, but do not interfere with CXCL12 levels, an important chemokine in the repair process.en
dc.description.affiliationDepartment of Biological Sciences Bauru School of Dentistry University of São Paulo, Al. Octávio Pinheiro Brisola, 9-75, Bauru, São Paulo, 17012-901
dc.description.affiliationDepartment of Physiology and Pathology Araraquara Dental School São Paulo State University, Araraquara, São Paulo
dc.description.affiliationCarlos Chagas Filho Institute of Biophysics Federal University of Rio de Janeiro, Rio de Janeiro, São Paulo
dc.description.affiliationUnespDepartment of Physiology and Pathology Araraquara Dental School São Paulo State University, Araraquara, São Paulo
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ)
dc.format.extent535-544
dc.identifierhttp://dx.doi.org/10.1902/jop.2012.120177
dc.identifier.citationJournal of Periodontology, v. 84, n. 4, p. 535-544, 2013.
dc.identifier.doi10.1902/jop.2012.120177
dc.identifier.issn0022-3492
dc.identifier.lattes4517484241515548
dc.identifier.scopus2-s2.0-84876149747
dc.identifier.urihttp://hdl.handle.net/11449/75023
dc.identifier.wosWOS:000317321100013
dc.language.isoeng
dc.relation.ispartofJournal of Periodontology
dc.relation.ispartofjcr3.392
dc.relation.ispartofsjr1,408
dc.rights.accessRightsAcesso restrito
dc.sourceScopus
dc.subjectCytokines
dc.subjectFibroblasts
dc.subjectGene silencing
dc.subjectPorphyromonas gingivalis
dc.subjectToll-like receptor 2
dc.subjectToll-like receptor 4
dc.subjectinterleukin 6
dc.subjectinterleukin 8
dc.subjectstromal cell derived factor 1
dc.subjecttoll like receptor 2
dc.subjecttoll like receptor 4
dc.subjectadolescent
dc.subjectadult
dc.subjectanalysis of variance
dc.subjectbiosynthesis
dc.subjectcell culture
dc.subjectcytology
dc.subjectfemale
dc.subjectfibroblast
dc.subjectgene silencing
dc.subjectgenetics
dc.subjectgingiva
dc.subjecthuman
dc.subjectinflammation
dc.subjectmale
dc.subjectmetabolism
dc.subjectnonparametric test
dc.subjectperiodontal ligament
dc.subjectRNA interference
dc.subjectsignal transduction
dc.subjectAdolescent
dc.subjectAdult
dc.subjectAnalysis of Variance
dc.subjectCells, Cultured
dc.subjectChemokine CXCL12
dc.subjectFemale
dc.subjectGene Knockdown Techniques
dc.subjectGingiva
dc.subjectHumans
dc.subjectInflammation
dc.subjectInterleukin-6
dc.subjectInterleukin-8
dc.subjectMale
dc.subjectPeriodontal Ligament
dc.subjectRNA Interference
dc.subjectSignal Transduction
dc.subjectStatistics, Nonparametric
dc.subjectToll-Like Receptor 2
dc.subjectToll-Like Receptor 4
dc.subjectYoung Adult
dc.titleToll-like receptor 2 knockdown modulates interleukin (IL)-6 and IL-8 but not stromal derived factor-1 (SDF-1/CXCL12) in human periodontal ligament and gingival fibroblastsen
dc.typeArtigo
dcterms.licensehttp://www.joponline.org/userimages/ContentEditor/1124388816475/Instructions_to_Authors.pdf
unesp.author.lattes4517484241515548[6]
unesp.author.orcid0000-0002-7455-6867[6]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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