Diabetes Enhances IL-17 Expression and Alters the Oral Microbiome to Increase Its Pathogenicity

Posted by: | July 13, 2017 | Comments

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•Diabetes increases periodontal bone resorption and tooth loss in mice
•Diabetic mice have increased periodontal inflammation and IL-17 levels
•Diabetic oral microbiota induces periodontitis in wild-type germ-free recipients
•Blocking IL-17 reduces the pathogenic effect of diabetic oral microbiota


Diabetes is a risk factor for periodontitis, an inflammatory bone disorder and the greatest cause of tooth loss in adults. Diabetes has a significant impact on the gut microbiota; however, studies in the oral cavity have been inconclusive. By 16S rRNA sequencing, we show here that diabetes causes a shift in oral bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mice is more pathogenic. Furthermore, treatment with IL-17 antibody decreases the pathogenicity of the oral microbiota in diabetic mice; when transferred to recipient germ-free mice, oral microbiota from IL-17-treated donors induced reduced neutrophil recruitment, reduced IL-6 and RANKL, and less bone resorption. Thus, diabetes-enhanced IL-17 alters the oral microbiota and renders it more pathogenic. Our findings provide a mechanistic basis to better understand how diabetes can increase the risk and severity of tooth loss.

Read Here: Cell Host & Microbe

E Xiao, Marcelo Mattos, Gustavo Henrique Apolinário Vieira, Shanshan Chen, Jôice Dias Corrêa, Yingying Wu, Mayra Laino Albiero, Kyle Bittinger, Dana T. Graves. DOI: http://dx.doi.org/10.1016/j.chom.2017.06.014.

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