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Inflammatory bowel diseases and brain-gut axis.

D Hollander1

  • 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

Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society
|April 13, 2004
PubMed
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.

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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).

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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.