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Comment
. 2018 Feb;15(2):92-95.
doi: 10.1038/cmi.2017.65. Epub 2017 Jul 31.

Gut microbiota metabolites for sweetening type I diabetes

Thamer Aljutaily  1 , Marta Consuegra-Fernández  2 , Fernando Aranda  2 , Francisco Lozano  2   3   4 , Eduardo Huarte  1
Affiliations
Comment

Gut microbiota metabolites for sweetening type I diabetes

Thamer Aljutaily et al. Cell Mol Immunol. 2018 Feb.
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Main experimental approach revealing the specific mechanisms of acetate and butyrate protection in T1D development. (a) NOD mice undergo exacerbated T1D in germ-free (GF) conditions. Oral administration of acetylated high-amylose maize starch (HAMSA) or butyrylated high-amylose maize starch (HAMSB) increased acetate or butyrate concentrations, respectively, which protected NOD mice from T1D development via independent mechanisms. Whereas HAMSA administration reduced specific IGRP (islet-specific antigen glucose-6-phospatase catalytic subunit-related protein) reactive CD8+ T-cells and induced a reduction in MHC-I and CD86 expression, HAMSB increased the Treg cell population. Splenic T-cells from NOD mice that were orally treated with HAMSB, when transferred into immunodeficient NOD-SCID mice, reduced T1D severity in receptor NOD-SCID mice. Fecal transplant of gut microbiota from NOD mice fed the HAMSA/HAMSB diet into GF NOD mice transferred diabetes protection. (b) NOD mice that express a transgene encoding the αβ TCR derived from a CD8+ T-cell clone specific against IGRP (NOD8.3) undergo acute T1D. The HAMSA diet inhibits the specific proliferation of IGRP reactive CD8+ T-cells NOD8.3 and, ultimately, T1D progression.
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