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

Abstract

<i>Chlamydia pneumoniae</i> 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 <i>C. pneumoniae</i> in inflammation and periodontal dis-ease. We found that <i>C. pneumoniae</i> was more frequently found in subgingival dental plaque obtained from periodontally diseased sites of the mouth versus healthy sites. The known periodontal pathogens, <i>Porphyromonas gingivalis</i> and <i>Aggregatibacter actinomycetemcomitans</i>, were also found in the plaque. In addition, <i>C. pneumoniae</i> could efficiently invade human gingival epithelial cells (GECs) <i>in vitro</i>, causing translocation of NF-κB to the nucleus along with increased secretion of mature IL-1β cytokine. Supernatants collected from <i>C. pneumoniae</i>-infected GECs showed increased activation of caspase-1 protein, which was significantly reduced when <i>nlrp3</i> gene expression was silenced using shRNA lentiviral vectors. Our results demonstrate that <i>C. pneumoniae</i> was found in higher levels in periodontitis patients compared to control pa-tients. Additionally, <i>C. pneumoniae</i> could infect GECs, leading to inflammation caused by activation of NF-κB and the NLRP3 inflammasome. We propose that the presence of <i>C. pneumoniae</i> in subgingival dental plaque may contribute to periodontal disease and could be used as a potential risk indicator of perio-dontal disease.