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Characterization of post-inflammatory irritable bowel syndrome animal model following acute colitis recovery

Title
Characterization of post-inflammatory irritable bowel syndrome animal model following acute colitis recovery
Authors
Jeong E.S.; Jung H.-K.; Choi E.; Yun K.; Lee A.; Kim Y.S.
Ewha Authors
정혜경
SCOPUS Author ID
정혜경scopus
Issue Date
2025
Journal Title
Scientific Reports
Citation
Scientific Reports vol. 15, no. 1
Keywords
Dextran sulfate sodium; Dysmotility; Irritable bowel syndrome; Low-grade inflammation; Microbiome; Murine model
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Irritable bowel syndrome (IBS) is a prevalent disorder with an unclear pathophysiology. This study aimed to investigate the features of dextran sulfate sodium (DSS)-induced low-grade inflammation using murine models of acute severe colitis (acute model) and chronic mild repeated colitis (chronic model), with potential implications for IBS research. The acute model was induced with 3% DSS for 5 days, followed by a 12-week recovery period. The chronic model involved administration of 0.5% DSS for 5 days, followed by a 5-day resting period, repeated thrice. We conducted comparative analyses to assess inflammation severity, intestinal motility, permeability, visceral hypersensitivity, and microbiome composition. In the acute model, mild leukocyte infiltration was observed, colonic transit time shortened at 12 weeks (P < 0.001), occludin expression decreased (P = 0.041), inflammatory cytokines, and transient receptor potential vanilloid 1 was upregulated in colonic mucosa (P < 0.050). In the chronic model, only mild inflammatory changes were noted. Microbiota analysis in the acute model revealed differences in microbial abundance and compositions (P = 0.001). The acute model demonstrated low-grade inflammation that caused gut dysmotility, altered permeability, and increased visceral hypersensitivity with notable microbial composition changes, potentially relevant to IBS phenotypes. © The Author(s) 2025.
DOI
10.1038/s41598-025-88981-7
Appears in Collections:
의과대학 > 의학과 > Journal papers
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