Douleurs inflammatoires - Publications Scientifiques

Dernière publication 03/05/2026

Akkermansia muciniphila drives viscero-visceral crosstalk via 5-HT3aR-mediated s

The comorbidity of overactive bladder (OAB) and irritable bowel syndrome (IBS) presents a major clinical challenge, with the underlying neural and...

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    [title] => Akkermansia muciniphila drives viscero-visceral crosstalk via 5-HT3aR-mediated s
    [paragraph] => Akkermansia muciniphila drives viscero-visceral crosstalk via 5-HT3aR-mediated sensitization of dichotomizing gut–bladder neurons
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Authors
Sun, Qi, Gao, Yubo, Zheng, Jun, Liao, Rulin, Jiang, Haotian, Zhu, Zhangrui, Xie, Ming, Yu, Yao, Zhu, Yuexuan, Li, Weijia, Shangguan, Wentai, Li, Leqian, Shi, Xinhang, Yang, Qishen, Zeng, Jiao, Wang, Zongwei, Zhao, Jie, Cheng, Bisheng, Wu, Peng

Lab
Journal
Experimental & Molecular Medicine
Abstract
The comorbidity of overactive bladder (OAB) and irritable bowel syndrome (IBS) presents a major clinical challenge, with the underlying neural and microbial mechanisms of the gut–bladder axis poorly understood. Here we aimed to delineate the complete causal pathway from a specific gut microorganism to bladder dysfunction and validate it as a therapeutic target. We combined analysis of human OAB–IBS cohorts with a postinflammatory mouse model, integrating retrograde neuronal tracing, multiomics (16S rDNA and metabolomics), fecal microbiota transplantation, urodynamics, dorsal root ganglion (DRG) electrophysiology and pharmacological and/or surgical interventions. We first confirmed a direct anatomical link, identifying dichotomized DRG neurons co-innervating the colon and bladder. Patients with OAB–IBS and mice exhibited a shared gut dysbiosis characterized by Akkermansia muciniphila enrichment. This comorbidity occurred in the absence of local bladder inflammation or urinary colonization with A. muciniphila, confirming a functional, noninfectious mechanism. Fecal microbiota transplantation of A. muciniphila or patient microbiota causally exacerbated visceral hypersensitivity, the OAB phenotype and DRG hyperexcitability. Mechanistically, A. muciniphila enrichment shunted host tryptophan metabolism toward the serotonin (5-HT) pathway. The resulting excess 5-HT acted on specifically upregulated colonic 5-HT3a receptors to drive neuronal sensitization. Crucially, pharmacological blockade of the colonic 5-HT3a receptor or surgical severing of the mesenteric nerves reversed the bladder dysfunction and visceral hypersensitivity. Our findings delineate a novel pathway wherein A. muciniphila drives functional gut–bladder comorbidity by promoting a gut-derived serotonergic signal that sensitizes shared afferent neurons, establishing the gut-specific 5-HT3a receptor as a key, druggable therapeutic target. Overactive bladder (OAB) and irritable bowel syndrome (IBS) often co-occur, affecting many adults and complicating treatment owing to unclear mechanisms. This study explores the gut–bladder connection, focusing on the role of the gut bacterium Akkermansia muciniphila. Researchers hypothesized that this bacterium influences OAB–IBS comorbidity by altering tryptophan metabolism, increasing serotonin production and activating sensory neurons. Using a mouse model, they demonstrated that A. muciniphila enrichment leads to increased serotonin levels and heightened neuron excitability, causing bladder dysfunction without local inflammation. The study found that blocking the serotonin receptor 5-HT3a or severing gut nerves alleviated symptoms, highlighting a neural pathway for gut–bladder communication. These findings suggest potential therapeutic targets, such as the 5-HT3a receptor, for treating OAB–IBS comorbidity, offering new insights into managing these disorders. Future research could explore microbiota modulation as a treatment strategy. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
Keywords/Topics
Bladder disease; Enteric nervous system; Experimental models of disease
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