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

Cássio Luiz Coutinho Almeida-da-Silva; Tamer Alpagot; Ye Zhu; Sonho Sierra Lee; Brian P Roberts; Shu-Chen Hung; Norina Tang; David M Ojcius

doi:10.15698/mic2019.04.674

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

Microb Cell. 2019 Mar 11;6(4):197-208. doi: 10.15698/mic2019.04.674.

Authors

Cássio Luiz Coutinho Almeida-da-Silva¹, Tamer Alpagot², Ye Zhu¹, Sonho Sierra Lee^{3

4}, Brian P Roberts⁵, Shu-Chen Hung¹, Norina Tang^{1

1}, David M Ojcius¹

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.

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.

Keywords: Chlamydia; caspase-1; inflammasome; inflammation; periodontitis.

Grants and funding

We acknowledge intramural grants from the University of the Pacific for funding this project. We thank Dr. Ozlem Yilmaz (Medical University of South Carolina) for the GECs, Dr. Moshe Arditi (University of California, Los Angeles) for a C. pneumoniae strain used in this study, and Dr. Mouchumi Bhattacharyya (University of the Pacific, Department of Mathematics) for her role in statistical assistance.