Abstract
Periodontitis is a prevalent chronic inflammatory disease triggered by a synergistic and dysbiotic microbiota present in the oral biofilm. This in vitro study is aimed at evaluating the regulation of cyclooxygenase (COX)2 expression and production by the periodontopathogen Filifactor alocis in human gingival fibroblastic (HGF-1) and monocytic (THP-1) cells and also at investigating the underlying cellular pathway mechanisms. HGF-1 and THP-1 cells were exposed either to F. alocis or to the proinflammatory cytokine tumor necrosis factor alpha (TNFα) for 1 and 2 d to examine the COX2 expression by qPCR. COX2 protein levels were evaluated by ELISA in F. alocis-stimulated cells. Both types of cells were also stimulated with a blocking toll-like receptor (TLR)2 antibody or specific inhibitors against MAPKs. F. alocis significantly (p < 0.05) increased COX2 at both transcriptional and protein levels in both HGF-1 and THP-1 cells. Moreover, the stimulatory effect of F. alocis on COX2 was more pronounced in HGF-1 cells in comparison to THP-1 cells. F. alocis upregulated the COX2 expression in a dose-dependent manner in both type cells at 1 d. TNFα also significantly (p < 0.05) increased the COX2 expression in both cells. After preincubation of HGF-1 and THP-1 cells either with a neutralizing anti-TLR2 antibody or with specific MAPK inhibitors, the F. alocis-upregulated COX2 expression was significantly (p < 0.05) suppressed at 1 d. Our in vitro study provides original evidence that F. alocis stimulates COX2 production in fibroblastic and monocytic cells through TLR2 and MAPK mechanisms, suggesting a role of this periodontopathogen in the etiopathogenesis of periodontitis.
Highlights
Periodontitis is a chronic inflammatory disease triggered by a synergistic and dysbiotic microbiota present in the oral biofilm
Both resident and infiltrating immune cells such as fibroblasts, monocytes, and macrophages are responsible for the increase in proinflammatory mediators like interleukin- (IL-) 1β, tumor necrosis factor alpha (TNFα), cyclooxygenase (COX)2, and matrix metalloproteinases
We investigated the regulation of COX2 in the presence and absence of the periodontopathogen F. alocis in HGF-1 cells
Summary
Periodontitis is a chronic inflammatory disease triggered by a synergistic and dysbiotic microbiota present in the oral biofilm Periodontopathogenic bacteria and their products activate the host immune response leading to an overproduction of proinflammatory mediators. Both resident and infiltrating immune cells such as fibroblasts, monocytes, and macrophages are responsible for the increase in proinflammatory mediators like interleukin- (IL-) 1β, tumor necrosis factor alpha (TNFα), cyclooxygenase (COX), and matrix metalloproteinases. These mediators play an important role in the hard and soft tissue destruction by modulating the inflammatory cascade in periodontitis [3]. Increased levels of COX2 and PGE2 have been demonstrated in saliva, gingiva, and gingival crevicular fluid of patients with periodontal disease [8,9,10,11,12,13]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
