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Chlamydia pneumoniae is present in the dental plaque of periodontitis patients and stimulates an inflammatory response in gingival epithelial cells.

ABSTRACT: Chlamydia pneumoniae is an airborne, Gram-negative, obligate intracellular bacterium which causes human respiratory infections and has been associated with atherosclerosis. Because individuals with periodontitis are at greater risk for atherosclerosis as well as respiratory infections, we in-vestigated the role of C. pneumoniae in inflammation and periodontal dis-ease. We found that C. pneumoniae was more frequently found in subgingival dental plaque obtained from periodontally diseased sites of the mouth versus healthy sites. The known periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were also found in the plaque. In addition, C. pneumoniae could efficiently invade human gingival epithelial cells (GECs) in vitro, causing translocation of NF-?B to the nucleus along with increased secretion of mature IL-1? cytokine. Supernatants collected from C. pneumoniae-infected GECs showed increased activation of caspase-1 protein, which was significantly reduced when nlrp3 gene expression was silenced using shRNA lentiviral vectors. Our results demonstrate that C. pneumoniae was found in higher levels in periodontitis patients compared to control pa-tients. Additionally, C. pneumoniae could infect GECs, leading to inflammation caused by activation of NF-?B and the NLRP3 inflammasome. We propose that the presence of C. pneumoniae in subgingival dental plaque may contribute to periodontal disease and could be used as a potential risk indicator of perio-dontal disease.

SUBMITTER: Almeida-da-Silva CLC

PROVIDER: S-EPMC6444558 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Chlamydia pneumoniae is present in the dental plaque of periodontitis patients and stimulates an inflammatory response in gingival epithelial cells.

Almeida-da-Silva Cássio Luiz Coutinho CLC Alpagot Tamer T Zhu Ye Y Lee Sonho Sierra SS Roberts Brian P BP Hung Shu-Chen SC Tang Norina N Ojcius David M DM

Microbial cell (Graz, Austria) 20190311 4

Chlamydia pneumoniae is an airborne, Gram-negative, obligate intracellular bacterium which causes human respiratory infections and has been associated with atherosclerosis. Because individuals with periodontitis are at greater risk for atherosclerosis as well as respiratory infections, we in-vestigated the role of C. pneumoniae in inflammation and periodontal dis-ease. We found that C. pneumoniae was more frequently found in subgingival dental plaque obtained from periodonta ...[more]

PMID: 30956972

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Project description:Histone deacetylases (HDACs) are important regulators of gene expression that are aberrantly regulated in several inflammatory and infectious diseases. HDAC inhibitors (HDACi) suppress inflammatory activation of various cell types through epigenetic and non-epigenetic mechanisms, and ameliorate pathology in a mouse model of periodontitis. Activation of gingival fibroblasts (GFs) significantly contributes to the development of periodontitis and the anaerobic bacterium Porphyromonas gingivalis plays a key role in driving chronic inflammation. Here, we analyzed the role of HDACs in inflammatory responses of GFs. Pan-HDACi suberoylanilide hydroxamic acid (SAHA) and/or ITF2357 (givinostat) significantly reduced TNFα- and P. gingivalis-inducible expression and/or production of a cluster of inflammatory mediators in healthy donor GFs (IL1B, CCL2, CCL5, CXCL10, COX2, and MMP3) without affecting cell viability. Selective inhibition of HDAC3/6, but not specific HDAC1, HDAC6, or HDAC8 inhibition, reproduced the suppressive effects of pan-HDACi on the inflammatory gene expression profile induced by TNFα and P. gingivalis, suggesting a critical role for HDAC3 in GF inflammatory activation. Consistently, silencing of HDAC3 expression with siRNA largely recapitulated the effects of HDAC3/6i on mRNA levels of inflammatory mediators in P. gingivalis-infected GFs. In contrast, P. gingivalis internalization and intracellular survival in GFs remained unaffected by HDACi. Activation of mitogen-activated protein kinases and NFκB signaling was unaffected by global or HDAC3/6-selective HDACi, and new protein synthesis was not required for gene suppression by HDACi. Finally, pan-HDACi and HDAC3/6i suppressed P. gingivalis-induced expression of IL1B, CCL2, CCL5, CXCL10, MMP1, and MMP3 in GFs from patients with periodontitis. Our results identify HDAC3 as an important regulator of inflammatory gene expression in GFs and suggest that therapeutic targeting of HDAC activity, in particular HDAC3, may be clinically beneficial in suppressing inflammation in periodontal disease.

Project description:Background/aimAtrial fibrillation (AF) is a major health problem and causes heart failure and stroke. Pathophysiological mechanisms indicate a link with oral health including periodontitis (PD), but supporting data are scarce. The aim was to investigate the link between features of oral health and the prevalence of AF.MethodsThis cross-sectional analysis of the Hamburg City Health Study included 5,634 participants with complete data on their PD and AF status. AF was assessed via self-reported questionnaire or medically diagnosed by standard 12-lead resting ECG. The oral health examination included full-mouth measurements of the dental plaque index (PI), the clinical attachment loss (CAL) at 6 sites per tooth, the bleeding on probing (BOP) and the decayed, missing and filled teeth (DMFT) index. Descriptive analyses for all variables stratified by the status of PD were performed. To test for an association between prevalent PD and prevalent AF, multivariable logistic regression models were used. Mediation analysis was used to test if interleukin-6 (IL-6) and/or C-reactive protein (CRP) mediated the association between PD and AF.ResultsAtrial fibrillation (prevalence: 5.6%) and the severity of PD (prevalence: moderate: 57.7%, severe: 18.9%) increased with age in men and women. Prevalent severe PD, CAL ≥3 mm, PI, and BOP were all associated with prevalent AF in unadjusted regression analysis. However, no association except for PI (odds ratio (OR): 1.22, 95% confidence interval (CI): 1.1-1.35, p<0.001) could be observed after adjusting for age, sex, high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), body mass index, diabetes, smoking, and educational level. Participants brushing their teeth at least twice daily had a lower AF prevalence compared with those brushing only once daily. Hs-CRP, IL-6, and the odds of AF increased as a function of PD severity grades in unadjusted analysis. However, neither the DMFT index nor IL-6 or CRP was associated with AF after adjusting for age and sex. Mediation analyses could not provide support for the hypothesis that IL-6 or CRP acted as mediator of the association between prevalent PD and prevalent AF.ConclusionThe study shows an association between prevalent AF and increased dental plaque levels indicated by a higher PI. In contrast, an association of prevalent PD with prevalent AF after adjustments for several confounders could not be demonstrated. Further studies are necessary to investigate the mechanisms underlying poor oral hygiene and AF as well as the influence of improved oral hygiene on AF onset.

Dataset Information

Chlamydia pneumoniae is present in the dental plaque of periodontitis patients and stimulates an inflammatory response in gingival epithelial cells.

Publications

<i>Chlamydia pneumoniae</i> is present in the dental plaque of periodontitis patients and stimulates an inflammatory response in gingival epithelial cells.

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