Transcriptomics

Dataset Information

0

An IFNg-dependent immune-endocrine circuit lowers blood glucose to potentiate the innate anti-viral immune response


ABSTRACT: Viral infection makes us feel sick. The extent of these changes to our metabolism are relative to the severity of disease. Whether blood glucose levels are subject to infection-induced modulation is largely unknown. Here we show that strong, non-lethal infection restricts systemic glucose availability which promotes the antiviral IFN-I response. Following systemic viral infection of mice, we find that IFNγ produced by γδ T cells directly stimulates pancreatic β-cells to increase glucose-induced insulin release. Subsequently, hyperinsulinemia lessens endogenous glucose output by the liver. Glucose restriction enhances type-I interferon production by curtailing lactate-mediated inhibition of IRF3 and NF-κB signaling. Induced hyperglycemia constrained IFN-I production and increased mortality upon infection. Our findings identify glucose restriction as a physiological mechanism to bring the body into a heightened state of responsiveness to viral pathogens. This immune-endocrine circuit is disrupted in hyperglycemia, which explains why patients with metabolic disease are more susceptible to viral infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE263599 | GEO | 2024/04/14

REPOSITORIES: GEO

Dataset's files

Source:
Action DRS
Other
Items per page:
1 - 1 of 1

Similar Datasets

2024-04-14 | GSE263600 | GEO
| 71713 | ecrin-mdr-crc
2024-06-30 | GSE263512 | GEO
2020-11-03 | PXD016398 | Pride
2019-05-07 | PXD012785 | Pride
2020-09-22 | GSE158267 | GEO
2016-03-16 | E-GEOD-79248 | biostudies-arrayexpress
2024-10-17 | GSE226242 | GEO
2016-03-16 | GSE79248 | GEO
2023-01-02 | E-MTAB-11781 | biostudies-arrayexpress