Dynamics of Gut Amyloid-Producing E coli May Play a Role in T1D Onset

There is a correlation between a high level of amyloid-producing Escherichia coli in the intestines, followed by their depletion due to prophage induction and the initiation of autoimmunity and type 1 diabetes (T1D) progression, according to research findings presented at the American Society for Microbiology (ASM) Microbe 2019, held June 20-24, 2019 in San Francisco, California.

Because gut microbiota plays a known role in T1D, researchers at the Human Microbiology Institute in New York City performed a longitudinal microbiome analysis in children age <3 years with human leukocyte antigens susceptibility to T1D. Results revealed an overlooked association between autoimmunity and the dynamics of gut amyloid-producing E coli.

Analysis revealed a different dynamic relationship in children with HLA-conferred susceptibility to T1D. E coli tended to disappear over time in patients with T1D and patients who were seroconverters, whereas it increased and did not change significantly over time in children without HLA-conferred susceptibility to T1D. E coli depletion was found before the appearance of antibodies, suggesting a role of E coli in disease onset.

Researchers noted that their in vitro study further “revealed a highly immunogenic complex (amyloid curli-DNA composites) released from E coli biofilms upon prophage induction, which triggered the production of type I [interferon] through the TLR2/9 stimulation of β-cells and, and autoimmune cascade through the TLR-2-MyD88-NF-kB pathway.”

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“Our study suggests that E coli biofilm-derived highly immunogenic amyloid curly-DNA complexes might be involved in the activation of a pro-diabetic pathway in children who are at a risk of T1D,” concluded the researchers.


Tetz G, Tetz V. A new developmental model for type 1 diabetes: an association between autoimmunity, the dynamics of gut amyloid-producing E. coli, & their phages. Presented at: ASM Microbe 2019; June 20-24, 2019; San Francisco, California. Poster P569.