Multi-omic analysis reveals brain-blood concordance and persistent neuroimmune reprogramming with stress and toxicant exposure in a mouse model of Gulf War Illness.

A Sasaki, K A Kelly, L T Michalovicz, D G Ashbrook, S Wijenayake, J P O'Callaghan, P O McGowan

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Article in Brain, behavior, & immunity - health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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7 authors.

A SasakiBiological Sciences, University of Toronto, Toronto, ON, Canada.

K A KellyCenters for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV, USA.

L T MichaloviczCenters for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV, USA.

D G AshbrookBiological Sciences, University of Toronto, Toronto, ON, Canada.

S WijenayakeBiological Sciences, University of Toronto, Toronto, ON, Canada.

J P O'CallaghanCenters for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV, USA.

P O McGowanBiological Sciences, University of Toronto, Toronto, ON, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gulf War Illness (GWI) is a chronic neuroimmune condition affecting veterans of the 1990-91 Gulf War. Current treatments primarily target symptom relief, and the biological mechanisms underlying GWI remain poorly understood. Using a validated mouse model of Gulf War Illness (GWI) combining corticosterone (CORT) and diisopropyl fluorophosphate (DFP) exposure to induce stress- and toxicant-related neuroimmune priming, we examined how prior exposure alters molecular responses to a subsequent immune challenge. Male mice were exposed to CORT and DFP with repeated intermittent CORT, followed by lipopolysaccharide (LPS) or saline to assess transcriptional and epigenetic changes in brain and blood. We analysed transcript abundance, chromatin accessibility, and DNA methylation in the hippocampus, frontal cortex, and blood at 6 h, 12 h and 24hrs after LPS challenge (3-4 mice per group). We identified widespread transcriptional changes and dynamic chromatin accessibility following LPS exposure, with DNA methylation modifications that persisted in the hippocampus and blood. Thirty-three genes, including

Indexed as

DNA methylation modificationsEpigenetic signaturesGulf War IllnessHippocampusNeuroinflammationStress and toxicant exposureTranscriptomics

Identifiers

PMID41993916

DOI10.1016/j.bbih.2026.101207

PMCPMC13081672

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