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"The presence of the bacterium Parabacteroides distasonis in the gut microbiome causes type 1 diabetes in a mouse model and seems to predict the onset of the disease in humans. This is likely because the microbe produces a peptide similar enough to part of an insulin molecule that it can lead to the production of insulin-targeted antibodies, priming the immune system to launch an attack against insulin and the cells that produce it. ...
Among the 222 records examined, infants younger than three years old who had P. distasonis in their gut microbiomes had a greater risk of developing type 1 diabetes later in life (in the Russian and Estonian cohorts, 100 percent of the infants who were eventually diagnosed with type 1 diabetes had signs of P. distasonis in their gut) ..."
Among the 222 records examined, infants younger than three years old who had P. distasonis in their gut microbiomes had a greater risk of developing type 1 diabetes later in life (in the Russian and Estonian cohorts, 100 percent of the infants who were eventually diagnosed with type 1 diabetes had signs of P. distasonis in their gut) ..."
From the abstract:
"Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic β-cells. One of the earliest aspects of this process is the development of autoantibodies and T cells directed at an epitope in the B-chain of insulin (insB:9–23). Analysis of microbial protein sequences with homology to the insB:9–23 sequence revealed 17 peptides showing >50% identity to insB:9–23. Of these 17 peptides, the hprt4–18 peptide, found in the normal human gut commensal Parabacteroides distasonis, activated both human T cell clones from T1D patients and T cell hybridomas from nonobese diabetic (NOD) mice specific to insB:9–23. Immunization of NOD mice with P. distasonis insB:9–23 peptide mimic or insB:9–23 peptide verified immune cross-reactivity. Colonization of female NOD mice with P. distasonis accelerated the development of T1D, increasing macrophages, dendritic cells, and destructive CD8+ T cells, while decreasing FoxP3+ regulatory T cells. ... Finally, analysis of human children gut microbiome data from a longitudinal DIABIMMUNE study revealed that seroconversion rates (i.e., the proportion of individuals developing two or more autoantibodies) were consistently higher in children whose microbiome harbored sequences capable of producing the hprt4–18 peptide compared to individuals who did not harbor it. Taken together, these data demonstrate the potential role of a gut microbiota-derived insB:9–23-mimic peptide as a molecular trigger of T1D pathogenesis."
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