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

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.