Porphyromonas gingivalis is an oral pathogen with the ability to induce oral dysbiosis and periodontal disease. Nevertheless, the mechanisms by which P. gingivalis could abrogate the host–microbe symbiotic relationship leading to oral dysbiosis remain unclear. We have recently demonstrated that P. gingivalis specifically increased the antimicrobial properties of oral epithelial cells, through a strong induction of the expression of PLA2-IIA in a mechanism that involves activation of the Notch-1 receptor. Moreover, gingival expression of PLA2-IIA was significantly increased during initiation and progression of periodontal disease in non-human primates and interestingly, those PLA2-IIA expression changes were concurrent with oral dysbiosis. In this chapter, we present an innovative hypothesis of a potential mechanism involved in P. gingivalis-induced oral dysbiosis and inflammation based on our previous observations and a robust body of literature that supports the antimicrobial and proinflammatory properties of PLA2-IIA as well as its role in other chronic inflammatory diseases.
|Title of host publication||Advances in Experimental Medicine and Biology|
|Number of pages||17|
|State||Published - 2019|
|Name||Advances in Experimental Medicine and Biology|
Bibliographical noteFunding Information:
Findings reported in this review were funded by NIH/NIDCR grant DE024804, NIH/ NIGMS P20GM103538 and College of Dentistry University of Kentucky. We thank Drs. Yongzheng Wu and Lhousseine Touqi from Institute Pasteur for kindly sharing the hPLA2-IIA-Tg mice as well as Drs. Jorge Frias (U. of Florida) and Sreenatha Kirakodu (U. of Kentucky) for their support in oral microbiome preliminary analysis. We also are grateful to Dr. Brittany Camenisch and Division of Periodontology for supporting the ongoing preliminary clinical study in salivary PLA2-IIA levels.
© 2019, Springer Nature Switzerland AG.
- Oral dysbiosis
- Oral epithelial cells
- P. gingivalis
- Periodontal disease
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology (all)