TY - JOUR
T1 - Diabetes Enhances IL-17 Expression and Alters the Oral Microbiome to Increase Its Pathogenicity
AU - Xiao, E.
AU - Mattos, Marcelo
AU - Vieira, Gustavo Henrique Apolinário
AU - Chen, Shanshan
AU - Corrêa, Jôice Dias
AU - Wu, Yingying
AU - Albiero, Mayra Laino
AU - Bittinger, Kyle
AU - Graves, Dana T.
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017/7/12
Y1 - 2017/7/12
N2 - 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.
AB - 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.
KW - IL-17
KW - bone loss
KW - diabetes
KW - dysbiosis
KW - microbiota
KW - osteoclast
KW - pathogen
KW - periodontitis
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U2 - 10.1016/j.chom.2017.06.014
DO - 10.1016/j.chom.2017.06.014
M3 - Article
C2 - 28704648
AN - SCOPUS:85030469022
SN - 1931-3128
VL - 22
SP - 120-128.e4
JO - Cell Host and Microbe
JF - Cell Host and Microbe
IS - 1
ER -