The human oral microbiota is altered in islet autoantibody positive individuals as well as those with type 1 diabetes

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Abstract Summary

Background

Homeostatic interactions between immune cells and microbes are essential for inducing tolerance, while disruptions to these interactions can modify disease susceptibility. Recent studies, including our own, suggest that commensals are important environmental components of type 1 diabetes (T1D). Most studies have focused on fecal microbiota and microbiota at other body sites have been less well studied. In individuals with T1D, it is completely unknown if the oral microbiota is perturbed, compared to healthy control subjects. Thus, the aim of our study was to investigate the composition of the oral microbiota in health and in T1D, as well as those "at risk", determined by islet autoantibody positivity.

Methods

We extracted bacterial DNA from mouth swabs of subjects from the Bart’s-Oxford Study (101 individuals with T1D, 11 "at risk" individuals and 115 non-diabetic control subjects) and conducted 16S rRNA sequencing. Sequence reads were filtered and those with >5000 reads/sample were further analyzed.

Results

We identified reduced alpha diversity between individuals with T1D vs healthy control subjects (p=0.0179).  There were no obvious changes in the Firmicutes/Bacteroidetes ratio between individuals with T1D and healthy control subjects.  However, the genera Capnocytophaga (Phylum of Bacteroidetes) and 3 Neisseriaceae genus members (Phylum of Proteobacteria) were significantly increased in individuals with T1D compared to control subjects (p<0.01).  Furthermore, we observed expansions or reductions in 3 Firmicutes members in ?at risk? individuals with islet autoantibodies compared with matched control subjects (p<0.05).  This suggests that the oral microbiota may be altered prior to T1D diagnosis and thus contribute to disease risk.

 

 Conclusion 

Our data demonstrate that individuals with T1D and those "at risk" have altered oral microbiota.  Further investigation will determine how these changes occur and if they can be used as a biomarker.

Submission ID :
IDS98112
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Yale University
Yale University
University of Bristol
University of Bristol
Cardiff University
University of Bristol
Yale University

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KEY DATES

Event dates:
Thursday 25 October - Monday 29 October 2018

Abstract submission deadline:
Monday 14 May 2018

Abstract notification:
July 2018

Early registration deadline:
Monday 3 September 2018

Registration deadline:
Monday 15 October 2018

Contact
British Society for Immunology
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