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

Authors:

Cássio Luiz Coutinho Almeida-da-Silva1, Tamer Alpagot2, Ye Zhu1, Sonho Sierra Lee3,4, Brian P. Roberts5, Shu-Chen Hung1, Norina Tang1,2 and David M. Ojcius1

doi: 10.15698/mic2019.04.674
Volume 6, pp. 197 to 208, published 11/03/2019.

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Affiliations:

1 Department of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA  94103, USA.

2 Department of Periodontics, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA  94103, USA.

3 College of Letters and Science, University of California, Berkeley, CA  94720, USA.

4 Program of Doctor of Dental Surgery, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA  94103, USA.

5 College of Letters and Science, University of California, Los Angeles, CA 90095, USA.

Keywords: 

Chlamydia, inflammasome, periodontitis, inflammation, caspase-1.

Corresponding Author(s):

David M. Ojcius, Department of Biomedical Sciences, University of the Pacific, Arthur A. Dugoni School of Dentistry, 155 Fifth Street, San Francisco, CA 94103, USA; dojcius@pacific.edu

Conflict of interest statement:

The authors declare that they have no conflicts of inter-est.

Please cite this article as:

Cássio Luiz Coutinho Almeida-da-Silva, Tamer Alpagot, Ye Zhu, Sonho Sierra Lee, Brian P. Roberts, Shu-Chen Hung, Norina Tang and David M. Ojcius (2019). Chlamydia pneumoniae is present in the dental plaque of periodontitis patients and stimu-lates an inflammatory response in gingival epithelial cells. Microbial Cell 6(4): 197-208. doi: 10.15698/mic2019.04.674

© 2019 Almeida-da-Silva et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and re-production in any medium, provided the original author and source are acknowledged.

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 investigated the role of C. pneumoniae in inflammation and periodontal disease. 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 patients. 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 periodontal disease.