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Therapeutic Evaluation of Fecal Microbiota Transplantation in an Interleukin 10-Deficient Mouse Model
Published on: April 6, 2022
Microbiota-immune-enteric nervous system interactions in functional constipation: a narrative review and
Dingzuo Ge1, Yu Zhan2, Yong Wen1
1Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Frontiers in Immunology
|July 17, 2026
Summary
Functional constipation (FC) and slow-transit constipation (STC) involve complex gut-brain interactions. A new Trigger-Gateway-Hub-Effector model organizes evidence on microbial, immune, and neural pathways, guiding future research and therapies.
Area of Science:
- Gastroenterology and Neurogastroenterology
- Microbiome Research
- Immunology
Background:
- Functional constipation (FC), especially slow-transit constipation (STC), is a complex gut-brain disorder with poor treatment response.
- Existing evidence suggests links between the gut microbiota, mucosal immunity, and the enteric nervous system (ENS), but mechanistic integration is incomplete.
Purpose of the Study:
- To propose a novel Trigger-Gateway-Hub-Effector framework to organize fragmented evidence on microbial-immune-neural interactions in FC/STC.
- To provide a hypothesis-generating model for understanding the pathophysiology of FC/STC.
Main Methods:
- Narrative review of existing literature.
- Conceptual model development (Trigger-Gateway-Hub-Effector framework).
Main Results:
- The framework identifies microbial metabolites as "Triggers," epithelial/immune changes as "Gateways," neuroimmune interactions as the "Hub," and ENS dysfunction as "Effectors."
- Limited direct evidence currently supports a complete causal chain, with many mechanisms inferred from preclinical data.
Conclusions:
- The proposed framework is a testable model, not a confirmed pathogenic sequence.
- Translational implications include systems biology approaches, evidence-weighted therapies, and mechanism-guided patient stratification.
- Future human studies integrating multi-omics and spatial analysis are needed to refine the model for precision therapies in FC/STC.
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