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Publication
cGAS/STING and innate brain inflammation following acute high-fat feeding.
Authors
Elzinga SE, Henn R, Murdock BJ, Kim B, Hayes JM, Mendelson F, Webber-Davis I,
Teener S, Pacut C, Lentz SI, Feldman EL
Submitted By
Submitted Externally on 11/2/2022
Status
Published
Journal
Frontiers in immunology
Year
2022
Date Published
Volume : Pages
13 : 1012594
PubMed Reference
36248795
Abstract
Obesity, prediabetes, and diabetes are growing in prevalence worldwide. These
metabolic disorders are associated with neurodegenerative diseases, particularly
Alzheimer's disease and Alzheimer's disease related dementias. Innate
inflammatory signaling plays a critical role in this association, potentially
via the early activation of the cGAS/STING pathway. To determine acute systemic
metabolic and inflammatory responses and corresponding changes in the brain, we
used a high fat diet fed obese mouse model of prediabetes and cognitive
impairment. We observed acute systemic changes in metabolic and inflammatory
responses, with impaired glucose tolerance, insulin resistance, and alterations
in peripheral immune cell populations. Central inflammatory changes included
microglial activation in a pro-inflammatory environment with cGAS/STING
activation. Blocking gap junctions in neuron-microglial co-cultures
significantly decreased cGAS/STING activation. Collectively these studies
suggest a role for early activation of the innate immune system both
peripherally and centrally with potential inflammatory crosstalk between neurons
and glia.
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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