dc.contributor.author | Berker, Ezel | |
dc.contributor.author | Kantarci, Alpdogan | |
dc.contributor.author | Hasturk, Hatice | |
dc.contributor.author | Van Dyke, Thomas E. | |
dc.date.accessioned | 2019-12-16T06:53:42Z | |
dc.date.available | 2019-12-16T06:53:42Z | |
dc.date.issued | 2013 | |
dc.identifier.issn | 0022-3492 | |
dc.identifier.uri | https://doi.org/10.1902/jop.2012.120422 | |
dc.identifier.uri | http://hdl.handle.net/11655/19149 | |
dc.description.abstract | Background: Chronic periodontitis (CP) is an inflammatory disease in which cytokines play a major role in the progression of disease. Anti-inflammatory cytokines (interleukin 4 [IL-4] and IL-10) were reported to be absent or reduced in diseased periodontal tissues, suggesting an imbalance between the proinflammatory and anti-inflammatory mediators. This study tests the hypothesis that there is cellular crosstalk mediated by proinflammatory and anti-inflammatory cytokines and that blocking proinflammatory cytokine (tumor necrosis factor-alpha [TNF-alpha] and IL-1) production will enhance antiinflammatory cytokine (IL-4 and IL-10) production from peripheral blood mononuclear cells (PBMCs) in response to Porphyromonas gingivalis. Methods: PBMCs were isolated from individuals diagnosed with CP or healthy individuals and cultured for 24 hours. Concanavalin A (ConA) was used as an activator of lymphocyte function. Live and heat-killed P. gingivalis or lipopolysaccharide from P. gingivalis were used as the bacterial stimulants. TNF-alpha and IL-1 production was neutralized by specific antibodies against TNF-alpha and IL-1a or IL-b. Culture supernatants were evaluated by enzyme-linked immunosorbent assay for TNF-alpha, IL-1b, IL-4, and IL-10 production. Results: Live P. gingivalis did not result in any significant IL-10 or IL-4 release, whereas heat-killed P. gingivalis led to a significant increase in IL-10 levels compared with unstimulated or live P. gingivalis-stimulated cells from both healthy individuals or those with CP. Overall, PBMCs from patients with CP produced significantly lower IL-10 in response to ConA and P. gingivalis, suggesting chronic suppression of the anti-inflammatory cytokine production. Blocking the proinflammatory cytokine response did not result in any substantial change in IL-10 or IL-4 response to live P. gingivalis. Blocking the proinflammatory cytokine response restored IL-10 production by cells from CP in response to P. gingivalis lipopolysaccharide. Conclusions: These findings suggest that PBMCs from patients with CP have suppressed anti-inflammatory cytokine production that can, in part, be restored by neutralizing proinflammatory cytokines. Monocytes are an important source of IL-10 production, and monocyte-derived IL-10 might play a regulatory role in the pathogenesis of CP. | |
dc.language.iso | en | |
dc.publisher | Wiley | |
dc.relation.isversionof | 10.1902/jop.2012.120422 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | Dentistry, Oral Surgery & Medicine | |
dc.title | Blocking Proinflammatory Cytokine Release Modulates Peripheral Blood Mononuclear Cell Response to Porphyromonas Gingivalis | |
dc.type | info:eu-repo/semantics/article | |
dc.type | info:eu-repo/semantics/publishedVersion | |
dc.relation.journal | Journal Of Periodontology | |
dc.contributor.department | Periodontoloji | |
dc.identifier.volume | 84 | |
dc.identifier.issue | 9 | |
dc.identifier.startpage | 29-Aug | |
dc.identifier.endpage | 1345 | |
dc.description.index | WoS | |