Expression and regulation of the NALP3 inflammasome complex in periodontal diseases

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dc.contributor.authorBostanci, N.
dc.contributor.authorEmingil, G.
dc.contributor.authorSaygan, B.
dc.contributor.authorTurkoglu, O.
dc.contributor.authorAtilla, G.
dc.contributor.authorCurtis, M. A.
dc.contributor.authorBelibasakis, G. N.
dc.date.accessioned2019-10-27T20:49:21Z
dc.date.available2019-10-27T20:49:21Z
dc.date.issued2009
dc.departmentEge Üniversitesien_US
dc.description.abstractPeriodontitis is an infectious process characterized by inflammation affecting the supporting structures of the teeth. Porphyromonas gingivalis is a major oral bacterial species implicated in the pathogenesis of periodontitis. Processing of interleukin (IL)-1 family cytokines is regulated by an intracellular innate immune response system, known as the NALP3 [nacht domain-, leucine-rich repeat-, and pyrin domain (PYD)-containing protein 3] inflammasome complex. The aim of the present study was to investigate by quantitative real-time polymerase chain reaction (PCR) the mRNA expression of NALP3, its effector molecule apoptosis associated speck-like protein (ASC), its putative antagonist NLRP2 (NLR family, PYD-containing protein 2), IL-1 beta and IL-18 (i) in gingival tissues from patients with gingivitis (n = 10), chronic periodontitis (n = 18), generalized aggressive periodontitis (n = 20), as well as in healthy subjects (n = 20), (ii) in vitro in a human monocytic cell line (Mono-Mac-6), in response to P. gingivalis challenge for 6 h. The clinical data indicate that NALP3 and NLRP2, but not ASC, are expressed at significantly higher levels in the three forms of inflammatory periodontal disease compared to health. Furthermore, a positive correlation was revealed between NALP3 and IL-1 beta or IL-18 expression levels in these tissues. The in vitro data demonstrate that P. gingivalis deregulates the NALP3 inflammasome complex in Mono-Mac-6 cells by enhancing NALP3 and down-regulating NLRP2 and ASC expression. In conclusion, this study reveals a role for the NALP3 inflammasome complex in inflammatory periodontal disease, and provides a mechanistic insight to the host immune responses involved in the pathogenesis of the disease by demonstrating the modulation of this cytokine-signalling pathway by bacterial challenge.en_US
dc.description.sponsorshipMedical Research CouncilMedical Research Council UK (MRC) [G0501478]en_US
dc.identifier.doi10.1111/j.1365-2249.2009.03972.xen_US
dc.identifier.endpage422en_US
dc.identifier.issn0009-9104
dc.identifier.issn1365-2249
dc.identifier.issue3en_US
dc.identifier.pmid19664151en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage415en_US
dc.identifier.urihttps://doi.org/10.1111/j.1365-2249.2009.03972.x
dc.identifier.urihttps://hdl.handle.net/11454/42861
dc.identifier.volume157en_US
dc.identifier.wosWOS:000268294500013en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofClinical and Experimental Immunologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectASCen_US
dc.subjectinterleukin-1 betaen_US
dc.subjectNALP3en_US
dc.subjectNLRP2en_US
dc.subjectperiodontitisen_US
dc.titleExpression and regulation of the NALP3 inflammasome complex in periodontal diseasesen_US
dc.typeArticleen_US

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