Neural and Glial Contributions to Mucosal Repair in Inflammatory Bowel Disease
- 1Ministry of Education Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae, Tianjin University of Traditional Chinese Medicine, 10 Poyanghu Road, Jinghai, Tianjin 301617, China
- 2Institute of Interdisciplinary Science, Tianjin University of Traditional Chinese Medicine, 10 Poyanghu Road, Tianjin 301617, China
Abstract
Mucosal healing is a central therapeutic goal in inflammatory bowel disease (IBD), yet control of inflammation does not invariably restore a durable and functional epithelium. Neural circuits are positioned to influence this discrepancy because they interact with epithelial, immune, stromal, vascular, and microbial components of the repair niche. However, evidence for neural regulation remains fragmented across studies of innervation, enteric glial cells, guidance cues, neurotransmitters, and neuro-immune signaling. Web of Science and PubMed were searched through October 2026 using terms covering IBD, mucosal repair, neural and glial signaling, and axon guidance; original mechanistic studies were prioritized and assessed by experimental model, cellular source and target, mechanistic intervention, and measured repair outcome. This review distinguishes acute restitution, barrier restoration, structural regeneration, and durable healing, and examines how sensory, autonomic, enteric neuronal, and glial pathways influence these outcomes across disease stages in IBD. It relates each pathway’s cellular source and response to neural perturbation to its disease context and highest measured repair endpoint. Semaphorin, netrin, Slit/Robo, and Eph/ephrin pathways may contribute to spatial organization, although most intestinal studies have not established that these effects depend on neural activity. By integrating repair endpoint, neural causality, disease stage, and cellular context, the review identifies key neural control points and experimental priorities for clinically meaningful translation.
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BibTeX
@article{cui2026neural,
title = {{Neural and Glial Contributions to Mucosal Repair in Inflammatory Bowel Disease}},
author = {Tianyi Cui and Yunhan Huang and Xiangqin Ou and Yang Yang and Jinglei Cui and Xinyue Dong and Xiumei Gao and Xin Zhao},
journal = {Biomolecules},
year = {2026},
month = oct,
doi = {10.3390/biom16111580},
url = {https://www.mdpi.com/2218-273X/16/11/1580},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Neural and Glial Contributions to Mucosal Repair in Inflammatory Bowel Disease
AU - Tianyi Cui
AU - Yunhan Huang
AU - Xiangqin Ou
AU - Yang Yang
AU - Jinglei Cui
AU - Xinyue Dong
AU - Xiumei Gao
AU - Xin Zhao
PY - 2026
DA - 2026/10/30
JO - Biomolecules
DO - 10.3390/biom16111580
UR - https://www.mdpi.com/2218-273X/16/11/1580
AB - Mucosal healing is a central therapeutic goal in inflammatory bowel disease (IBD), yet control of inflammation does not invariably restore a durable and functional epithelium. Neural circuits are positioned to influence this discrepancy because they interact with epithelial, immune, stromal, vascular, and microbial components of the repair niche. However, evidence for neural regulation remains fragmented across studies of innervation, enteric glial cells, guidance cues, neurotransmitters, and neuro-immune signaling. Web of Science and PubMed were searched through October 2026 using terms covering IBD, mucosal repair, neural and glial signaling, and axon guidance; original mechanistic studies were prioritized and assessed by experimental model, cellular source and target, mechanistic intervention, and measured repair outcome. This review distinguishes acute restitution, barrier restoration, structural regeneration, and durable healing, and examines how sensory, autonomic, enteric neuronal, and glial pathways influence these outcomes across disease stages in IBD. It relates each pathway’s cellular source and response to neural perturbation to its disease context and highest measured repair endpoint. Semaphorin, netrin, Slit/Robo, and Eph/ephrin pathways may contribute to spatial organization, although most intestinal studies have not established that these effects depend on neural activity. By integrating repair endpoint, neural causality, disease stage, and cellular context, the review identifies key neural control points and experimental priorities for clinically meaningful translation.
SN - 2218-273X
ER -