ArticleJournal of neurochemistry2017
Corticosterone primes the neuroinflammatory response to Gulf War Illness-relevant organophosphates independently of acetylcholinesterase inhibition.
Article in Journal of neurochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Corticosteroid Usage in Modeling Gulf War Illness in Pre-Clinical Models: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Multi-omic analysis reveals brain-blood concordance and persistent neuroimmune reprogramming with stress and toxicant exposure in a mouse model of Gulf War Illness.Brain, behavior, & immunity - health · 2026Article
- Chlorpyrifos and Chlorpyrifos-Oxon: A Widening Spectrum of Toxicity.International journal of molecular sciences · 2026Review
- GM1 and GD3 Gangliosides Attenuate Diisopropylfluorophosphate-Induced NGF-TrkA and BDNF-TrkB Signaling Dysfunction.ACS chemical neuroscience · 2026Article
- Article
- Evaluation of the Therapeutic Potential of Synthetic Growth Hormone-Releasing Hormone Antagonist MIA-690 as a Cognitive Modulator in a Mouse Model of Gulf War Illness.International journal of molecular sciences · 2025Article
- Nerve agent exposure and physiological stress alter brain microstructure and immune profiles after inflammatory challenge in a long-term rat model of Gulf War Illness.Brain, behavior, & immunity - health · 2024Article
- Endocrine-Disrupting Chemicals, Hypothalamic Inflammation and Reproductive Outcomes: A Review of the Literature.International journal of molecular sciences · 2024Review
- Acute exposure to diisopropylfluorophosphate in mice results in persistent cognitive deficits and alterations in senescence markers in the brain.Frontiers in neuroscience · 2024Article
- Mitochondrial impairment but not peripheral inflammation predicts greater Gulf War illness severity.Scientific reports · 2023Article
- A Projectile Concussive Impact Model Produces Neuroinflammation in Both Mild and Moderate-Severe Traumatic Brain Injury.Brain sciences · 2023Article
- Epigenetic analysis in a murine genetic model of Gulf War illness.Frontiers in toxicology · 2023Article
- Impact of gulf war toxic exposures after mild traumatic brain injury.Acta neuropathologica communications · 2022Article
- Genomic Basis for Individual Differences in Susceptibility to the Neurotoxic Effects of Diesel Exhaust.International journal of molecular sciences · 2022Article
- Oral Nano-Curcumin in a Model of Chronic Gulf War Illness Alleviates Brain Dysfunction with Modulation of Oxidative Stress, Mitochondrial Function, Neuroinflammation, Neurogenesis, and Gene Expression.Aging and disease · 2022Article
- A pilot reverse virtual screening study suggests toxic exposures caused long-term epigenetic changes in Gulf War Illness.Computational and structural biotechnology journal · 2022Article
- A review of chemical warfare agents linked to respiratory and neurological effects experienced in Gulf War Illness.Inhalation toxicology · 2022Review
- Veteran-derived cerebral organoids display multifaceted pathological defects in studies on Gulf War Illness.Frontiers in cellular neuroscience · 2022Article
- Brain-Specific Increase in Leukotriene Signaling Accompanies Chronic Neuroinflammation and Cognitive Impairment in a Model of Gulf War Illness.Frontiers in immunology · 2022Article
- The β-adrenergic receptor blocker and anti-inflammatory drug propranolol mitigates brain cytokine expression in a long-term model of Gulf War Illness.Life sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gulf War Illness (GWI) is a chronic multi-symptom disorder affecting veterans of the 1991 Gulf War. Among the symptoms of GWI are those associated with sickness behavior, observations suggestive of underlying neuroinflammation. We have shown that exposure of mice to the stress hormone, corticosterone (CORT), and to diisopropyl fluorophosphate (DFP), as a nerve agent mimic, results in marked neuroinflammation, findings consistent with a stress/neuroimmune basis of GWI. Here, we examined the contribution of irreversible and reversible acetylcholinesterase (AChE) inhibitors to neuroinflammation in our mouse model of GWI. Male C57BL/6J mice received 4 days of CORT (400 mg/L) in the drinking water followed by a single dose of chlorpyrifos oxon (CPO; 8 mg/kg, i.p.), DFP (4 mg/kg, i.p.), pyridostigmine bromide (PB; 3 mg/kg, i.p.), or physostigmine (PHY; 0.5 mg/kg, i.p.). CPO and DFP alone caused cortical and hippocampal neuroinflammation assessed by qPCR of tumor necrosis factor-alpha, IL-6, C-C chemokine ligand 2, IL-1β, leukemia inhibitory factor and oncostatin M; CORT pretreatment markedly augmented these effects. Additionally, CORT exposure prior to DFP or CPO enhanced activation of the neuroinflammation signal transducer, signal transducer and activator of transcription 3 (STAT3). In contrast, PHY or PB alone or with CORT pretreatment did not produce neuroinflammation or STAT3 activation. While all of the CNS-acting AChE inhibitors (DFP, CPO, and PHY) decreased brain AChE activity, CORT pretreatment abrogated these effects for the irreversible inhibitors. Taken together, these findings suggest that irreversible AChE inhibitor-induced neuroinflammation and particularly its exacerbation by CORT, result from non-cholinergic effects of these compounds, pointing potentially to organophosphorylation of other neuroimmune targets.
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