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Cross-talk between the gut microbiota and the host immune system regulates host metabolism, and its dysregulation can cause metabolic disease. Here, we show that the gut microbe  Akkermansia muciniphila  can mediate negative effects of IFNγ on glucose tolerance. In IFNγ-deficient mice,  A. muciniphila  is significantly increased and restoration of IFNγ levels reduces  A. muciniphila  abundance. We further show that IFNγ-knockout mice whose microbiota does not contain  A. muciniphila  do not show improvement in glucose tolerance and adding back  A. muciniphila  promoted enhanced glucose tolerance. We go on to identify Irgm1 as an IFNγ-regulated gene in the mouse ileum that controls gut  A. muciniphila  levels.  A. muciniphila  is also linked to IFNγ-regulated gene expression in the intestine and glucose parameters in humans, suggesting that this trialogue between IFNγ,  A. muciniphila  and glucose tolerance might be an evolutionally conserved mechanism regulating metabolic health in mice and humans.

Akkermansia muciniphila mediates negative effects of IFNγ on glucose metabolism