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

E. Xiao, Marcelo Mattos, Gustavo Henrique Apolinário Vieira, Shanshan Chen, Jôice Dias Corrêa, Yingying Wu, Mayra Laino Albiero, Kyle Bittinger, Dana T. Graves

Research output: Contribution to journalArticlepeer-review

227 Scopus citations


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. Diabetes increases periodontal disease, a major cause of tooth loss. Xiao et al. demonstrated, by transfer to germ-free mice, that oral microbiota from diabetic mice induced more periodontal inflammation and bone loss than microbiota from normal mice. Diabetes increased the pathogenicity of the oral microbiota through an IL-17-mediated mechanism.

Original languageEnglish
Pages (from-to)120-128.e4
JournalCell Host and Microbe
Issue number1
StatePublished - Jul 12 2017

Bibliographical note

Publisher Copyright:
© 2017 Elsevier Inc.


  • IL-17
  • bone loss
  • diabetes
  • dysbiosis
  • microbiota
  • osteoclast
  • pathogen
  • periodontitis

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Virology


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