biostudies-literatureKozlova EVNIDDK NIH HHSNIAID NIH HHSNIGMS NIH HHS120153https://www.ebi.ac.uk/biostudies/studies/S-EPMC9048156biostudies-literatureUnknown288<h4>Aims</h4>To characterize neuroinflammatory and gut dysbiosis signatures that accompany exaggerated exercise fatigue and cognitive/mood deficits in a mouse model of Gulf War Illness (GWI).<h4>Methods</h4>Adult male C57Bl/6N mice were exposed for 28 d (5 d/wk) to pyridostigmine bromide (P.O.) at 6.5 mg/kg/d, b.i.d. (GW1) or 8.7 mg/kg/d, q.d. (GW2); topical permethrin (1.3 mg/kg), topical N,N-diethyl-meta-toluamide (33%) and restraint stress (5 min). Animals were phenotypically evaluated as described in an accompanying article [124] and sacrificed at 6.6 months post-treatment (PT) to allow measurement of brain neuroinflammation/neuropathic pain gene expression, hippocampal glial fibrillary acidic protein, brain Interleukin-6, gut dysbiosis and serum endotoxin.<h4>Key findings</h4>ComparedLife sciencesInduction of distinct neuroinflammatory markers and gut dysbiosis by differential pyridostigmine bromide dosing in a chronic mouse model of GWI showing persistent exercise fatigue and cognitive impairment.PMC9048156R01 AI157106R01 AI153314R35 GM124724R01 DK091281R01 DK130373R21 AI152017Piamthai VCarabelli BMcCole DFBishay AECrawford MSCurras-Collazo MCZur Nieden NIDenys MELiu RKozlova EVMacbeth JCHsiao AfalseInduction of distinct neuroinflammatory markers and gut dysbiosis by differential pyridostigmine bromide dosing in a chronic mouse model of GWI showing persistent exercise fatigue and cognitive impairment.<h4>Aims</h4>To characterize neuroinflammatory and gut dysbiosis signatures that accompany exaggerated exercise fatigue and cognitive/mood deficits in a mouse model of Gulf War Illness (GWI).<h4>Methods</h4>Adult male C57Bl/6N mice were exposed for 28 d (5 d/wk) to pyridostigmine bromide (P.O.) at 6.5 mg/kg/d, b.i.d. (GW1) or 8.7 mg/kg/d, q.d. (GW2); topical permethrin (1.3 mg/kg), topical N,N-diethyl-meta-toluamide (33%) and restraint stress (5 min). Animals were phenotypically evaluated as described in an accompanying article [124] and sacrificed at 6.6 months post-treatment (PT) to allow measurement of brain neuroinflammation/neuropathic pain gene expression, hippocampal glial fibrillary acidic protein, brain Interleukin-6, gut dysbiosis and serum endotoxin.<h4>Key findings</h4>Compared2022-01-01T00:00:00Z2022 Jan2026-05-31T21:54:27.529Z2024-11-09T12:05:43.036ZS-EPMC90481563480151310.1016/j.lfs.2021.120153