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Inflammatory bowel diseases and brain-gut axis.
1UCLA School of Medicine and Broad Medical Research Program, The Eli and Edythe L. Broad Foundation, Twelfth Floor, Los Angeles, California 90024-6532, USA. dhollander@broadmedical.org
Summary
High stress significantly increases inflammatory bowel disease (IBD) recurrence by 90% in patients. Stress impacts gut permeability and inflammation via brain-gut interactions, potentially reactivating Crohn's disease.
Area of Science:
- Gastroenterology
- Neuroimmunology
- Molecular Biology
Background:
- Inflammatory bowel disease (IBD) involves chronic gut inflammation.
- The role of stress in exacerbating IBD is increasingly recognized.
- Brain-gut interactions are critical in modulating intestinal health.
Purpose of the Study:
- To review the influence of stress on inflammation in IBD.
- To explore stress mediators and their impact on gut permeability.
- To elucidate the role of stress in IBD pathogenesis and reactivation.
Main Methods:
- Review of experimental colitis models in rats.
- Longitudinal study of stable IBD patients over five years.
- Analysis of stress mediators (e.g., VIP, TNF-alpha) and intestinal permeability markers (e.g., Cr-EDTA, HRP).
Main Results:
- Stress reactivated experimental colitis.
- IBD patients with high prolonged stress had 90% recurrence vs. 40% in low-stress patients.
- Stress increased intestinal permeability, including M-cells and Paneth cells, potentially linking to Crohn's disease via NOD2.
Conclusions:
- Stress exacerbates intestinal inflammation in IBD through brain-gut interactions.
- Mediators like VIP, TNF-alpha, and catecholamines are involved.
- Stress may contribute to the initiation or relapse of IBD, particularly Crohn's disease.