Potassium is a key signal in host-microbiome dysbiosis in periodontitis

Susan Yost, Ana E. Duran-Pinedo, Keerthana Krishnan, Jorge Frias-Lopez

Dysbiosis, or the imbalance in the structural and/or functional properties of the microbiome, is at the origin of important infectious inflammatory diseases such as inflammatory bowel disease (IBD) and periodontal disease. Periodontitis is a polymicrobial inflammatory disease that affects a large proportion of the world’s population and has been associated with a wide variety of systemic health conditions, such as diabetes, cardiovascular and respiratory diseases. Dysbiosis has been identified as a key element in the development of the disease. However, the precise mechanisms and environmental signals that lead to the initiation of dysbiosis in the human microbiome are largely unknown. In a series of previous in vivo studies using meta transcriptomic analysis of periodontitis and its progression we identified several functional signatures that were highly associated with the disease. Among them, potassium ion transport appeared to be key in the process of pathogenesis. To confirm its importance we performed a series of in vitro experiments, in which we demonstrated that potassium levels a increased the virulence of the oral community as a whole and at the same time altering the immune response of gingival epithelium, increasing the production of TNF-α and reducing the expression of IL-6 and the anti microbial peptide human ß-defensin 3(hBD-3).These results indicate that levels of potassium in the periodontal pocket could be an important element in of dysbiosis in the oral microbiome. They are a starting point for the  identification of key environmental signals that modify the behavior of the oral microbiome from a symbiotic community to a dysbiotic one.


Dysbiosis, EpiGingival (GIN-100), Interleukin-6 (IL-6), oral microbiome, TNF-a, HBD-3, periodontal disease, periodontitis, Interferon-gamma, IFN-g, IL-10, IL-1b, IL-17a

Materials Tested

dental plague, potassium

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