Akkermansia muciniphila mediates negative effects of IFNγ on glucose metabolism.
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.
Duke Scholars
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- Verrucomicrobia
- Mice, Knockout
- Mice, Inbred C57BL
- Interferon-gamma
- Ileum
- Humans
- Glucose
- Gene Expression
- Gastrointestinal Microbiome
- GTP-Binding Proteins
Citation
Published In
DOI
EISSN
Publication Date
Volume
Start / End Page
Location
Related Subject Headings
- Verrucomicrobia
- Mice, Knockout
- Mice, Inbred C57BL
- Interferon-gamma
- Ileum
- Humans
- Glucose
- Gene Expression
- Gastrointestinal Microbiome
- GTP-Binding Proteins