English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Gulf War Illness ( GWI ) is a multi‐symptom disorder with features characteristic of persistent sickness behavior. Among conditions encountered in the Gulf War ( GW ) theater were physiological stressors (e.g., heat/cold/physical activity/sleep deprivation), prophylactic treatment with the reversible  AC hE inhibitor, pyridostigmine bromide (PB), the insect repellent,  N , N ‐diethyl‐meta‐toluamide (DEET), and potentially the nerve agent, sarin. Prior exposure to the anti‐inflammatory glucocorticoid, corticosterone ( CORT ), at levels associated with high physiological stress, can paradoxically prime the  CNS  to produce a robust proinflammatory response to neurotoxicants and systemic inflammation; such neuroinflammatory effects can be associated with sickness behavior. Here, we examined whether  CORT  primed the  CNS  to mount neuroinflammatory responses to  GW  exposures as a potential model of  GWI . Male C57 BL /6 mice were treated with chronic (14 days) PB/ DEET, subchronic (7–14 days)  CORT , and acute exposure (day 15) to diisopropyl fluorophosphate ( DFP ), a sarin surrogate and irreversible  AC hE inhibitor.  DFP  alone caused marked brain‐wide neuroinflammation assessed by  qPCR  of tumor necrosis factor‐α,  IL 6, chemokine (C‐C motif) ligand 2,  IL ‐1β, leukemia inhibitory factor, and oncostatin M. Pre‐treatment with high physiological levels of  CORT  greatly augmented (up to 300‐fold) the neuroinflammatory responses to  DFP . Anti‐inflammatory pre‐treatment with minocycline suppressed many proinflammatory responses to  CORT + DFP . Our findings are suggestive of a possible critical, yet unrecognized interaction between the stressor/environment of the  GW  theater and agent exposure(s) unique to this war. Such exposures may in fact prime the  CNS  to amplify future neuroinflammatory responses to pathogens, injury, or toxicity. Such occurrences could potentially result in the prolonged episodes of sickness behavior observed in  GWI .Gulf War (GW) veterans were exposed to stressors, prophylactic medicines and, potentially, nerve agents in theater. Subsequent development of GW Illness, a persistent multi‐symptom disorder with features characteristic of sickness behavior, may be caused by priming of the CNS resulting in exaggerated neuroinflammatory responses to pathogens/insults. Nerve agent, diisopropyl fluorophosphate (DFP), produced a neuroinflammatory response that was exacerbated by pre‐treatment with levels of corticosterone simulating heightened stressor conditions. While prophylactic treatments reduced DFP‐induced neuroinflammation, this effect was negated when those treatments were combined with corticosterone.

Corticosterone primes the neuroinflammatory response to DFP in mice: potential animal model of Gulf War Illness