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dc.contributor.authorHernández-Caldera A.
dc.contributor.authorVernal R.
dc.contributor.authorParedes R.
dc.contributor.authorVeloso-Matta P.
dc.contributor.authorAstorga J.
dc.contributor.authorHernández M.
dc.date.accessioned2020-09-02T22:20:02Z
dc.date.available2020-09-02T22:20:02Z
dc.date.issued2018
dc.identifier10.1111/iej.12872
dc.identifier.citation51, 6, 632-640
dc.identifier.issn01432885
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4851
dc.descriptionAim: To characterize the potential of human periodontal ligament fibroblasts (HPLF) to synthesize CRP and Th-related cytokines in response to IL-6 in periodontal health and apical inflammation. Methodology: Primary HPLF stimulated with IL-6, soluble(s) IL-6 receptor (R) and controls were assayed for CRP, Th1, Th2, Th17 and Treg-related cytokines by quantitative real-time PCR and ELISA, respectively. IL-6R mRNA expression and its soluble protein levels were screened in HPLF cultures, and ex vivo samples of healthy periodontal ligaments (n = 5) and apical lesions (n = 13). Data were analysed with ANOVA or unpaired t-test. Results: 0.5 ng mL−1 IL-6 plus 1 ng mL−1 of its soluble receptor (sIL-6R) for 24 h was effective in inducing CRP production. IL-6 alone had a mild dose-dependent effect; co-stimulation with sIL-6R significantly enhanced this effect, whereas it was completely abolished by the addition of IL-6R blocking antibody (P < 0.05). Similarly, higher mRNA expression and protein levels of Th1, Th17 and partially Treg-related cytokines were found for IL-6 combined with its soluble receptor versus the nonstimulated group and IL-6R antibody (P < 0.05). IL-6R mRNA expression was slightly induced by IL-6 compared to THP-1 cells, but sILR-6 protein could not be detected in HPLF. High sIL-6R levels were detected in apical lesions and were immunolocalized to mononuclear inflammatory cells and proliferating epithelium. Conclusion: IL-6 trans-signalling induced Th1 and Th17-related cytokines and represents an extra-hepatic mechanism for PCR synthesis in human periodontal ligament fibroblasts, contributing to explain the bone-destructive phenotype of apical lesions and eventually its systemic complications. © 2017 International Endodontic Journal. Published by John Wiley & Sons Ltd
dc.language.isoen
dc.publisherBlackwell Publishing Ltd
dc.subjectC-reactive protein
dc.subjectinterleukin-6
dc.subjectinterleukin-6 receptor
dc.subjectperiodontal ligament fibroblast
dc.subjectTh cytokines
dc.subjectautacoid
dc.subjectC reactive protein
dc.subjectinterleukin 1
dc.subjectinterleukin 17
dc.subjectinterleukin 2
dc.subjectinterleukin 6
dc.subjectinterleukin 6 receptor
dc.subjectbiosynthesis
dc.subjectcell culture
dc.subjectcytology
dc.subjectenzyme linked immunosorbent assay
dc.subjectfibroblast
dc.subjecthuman
dc.subjectmetabolism
dc.subjectperiodontal ligament
dc.subjectphysiology
dc.subjectreal time polymerase chain reaction
dc.subjectsignal transduction
dc.subjectC-Reactive Protein
dc.subjectCells, Cultured
dc.subjectEnzyme-Linked Immunosorbent Assay
dc.subjectFibroblasts
dc.subjectHumans
dc.subjectInflammation Mediators
dc.subjectInterleukin-1
dc.subjectInterleukin-17
dc.subjectInterleukin-2
dc.subjectInterleukin-6
dc.subjectPeriodontal Ligament
dc.subjectReal-Time Polymerase Chain Reaction
dc.subjectReceptors, Interleukin-6
dc.subjectSignal Transduction
dc.titleHuman periodontal ligament fibroblasts synthesize C-reactive protein and Th-related cytokines in response to interleukin (IL)-6 trans-signalling
dc.typeArticle


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