CHRONIC COLITIS ALTERS BRAIN ACTIVITY BY INDUCING HMGB1-MEDIATED PYROPTOSIS IN MICE
نویسندگان
چکیده
Abstract BACKGROUND AND AIM Chronic gut inflammation such as inflammatory bowel diseases is thought being associated with neurodegenerative in humans. The direct evidence for and the underlying mechanism of this brain-gut interaction, however, remain elusive. METHODS We used manganese-enhanced magnetic resonance imaging (MEMRI) to assess brain functional activity from awake freely moving mice. As a mouse model chronic colitis, mice were treated three cycles dextran sulfate sodium. performed passive avoidance test, which fear-motivated test that assesses short-term long-term memory. Mouse hippocampus tissues microglial cells subjected GC-MS, immunofluorescence staining, ELISA, immunoblotting analysis examine how inflamed linked pathology. RESULTS found manganese ion uptake, indicative Ca2+ influx into neuronal cells, accumulation are dramatically reduced colitis compared control Long-term memory declined Neuroinflammatory signals, including IL-1β production activation Caspase-1, Caspase-11, Gasdermin (GSDM), induced High-mobility group box 1 (HMGB1) level elevated both serum mice; lipopolysaccharide (LPS) levels at low without significant changes these samples. blood-brain barrier permeability increased In presence LPS, accordingly, HMGB1 treatment induces Caspase-11 GSDM cell line SIM-A9. CONCLUSION Our findings suggest released intestine may move through blood circulatory system; conjunction endogenous can subsequently activate Caspase-mediated responses brain. This study implies alter
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ژورنال
عنوان ژورنال: Inflammatory Bowel Diseases
سال: 2022
ISSN: ['1078-0998', '1536-4844']
DOI: https://doi.org/10.1093/ibd/izac015.089