Microbiota dysbiosis and mucosal hyperinnervation contribute to intestinal hyperalgesia in a mouse model of postinfectious irritable bowel syndrome

American Journal of Physiology-Gastrointestinal and Liver Physiology 2026 Open access

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Authors: Li-Yu Lin, Yu‐Hsuan Lin, Chia-Hung Tu, Ming-Shiang Wu, WH Kuo, Chin‐Hung Sun, Ling‐Wei Hsin, Linda Chia‐Hui Yu
DOI: 10.1152/ajpgi.00007.2026
Cited by: 1
References: 76

Abstract

A mouse model of postinfectious IBS was developed using dual triggers of Giardia postinfection and water avoidance stress to mimic diverse risk factors. Rifaximin treatment reduced intestinal hyperalgesia and was associated with decreased mucosal neurite outgrowth and brain-derived neurotrophic factor (BDNF) expression. BDNF activation induced nerve fiber elongation and upregulated 5-HT 7 expression via separate signaling pathways. Analgesic combinations of RFX and a 5-HT 7 receptor antagonist reduced intestinal nociception to baseline.

Fields of Study & Subjects

Gastrointestinal motility and disorders Gut microbiota and health Clostridium difficile and Clostridium perfringens research

Publication details

Journal / source
American Journal of Physiology-Gastrointestinal and Liver Physiology
Publisher
American Physiological Society
Volume
331
Issue
2
Pages
G165–G182
Publication date
29 June 2026
Language
EN