ORCiD
David M. Ojcius: 0000-0003-1461-4495; Cassio Almeida-da-Silva: 0000-0001-9173-7208
Department
Biomedical Sciences
Document Type
Article
Publication Title
Microbial Cell
ISSN
2311-2638
Volume
6
Issue
4
DOI
10.15698/mic2019.04.674
First Page
197
Last Page
208
Publication Date
3-11-2019
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-κB to the nucleus along with increased secretion of mature IL-1β 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-κB 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.
Recommended Citation
Almeida-da-Silva, C. L.,
Alpagot, T.,
Zhu, Y.,
Lee, S. S.,
Roberts, B. P.,
Hung, S.,
Tang, N.,
&
Ojcius, D. M.
(2019).
Chlamydia pneumoniae is present in the dental plaque of periodontitis patients and stimulates an inflammatory response in gingival epithelial cells.
Microbial Cell, 6(4), 197–208.
DOI: 10.15698/mic2019.04.674
https://scholarlycommons.pacific.edu/dugoni-facarticles/459
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
