| Literature DB >> 28704648 |
E Xiao1, Marcelo Mattos2, Gustavo Henrique Apolinário Vieira3, Shanshan Chen4, Jôice Dias Corrêa5, Yingying Wu4, Mayra Laino Albiero6, Kyle Bittinger7, Dana T Graves8.
Abstract
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.Entities:
Keywords: IL-17; bone loss; diabetes; dysbiosis; microbiota; osteoclast; pathogen; periodontitis
Mesh:
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Year: 2017 PMID: 28704648 PMCID: PMC5701758 DOI: 10.1016/j.chom.2017.06.014
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023