Abstract

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder defined by ROME IV criteria as pain in the lower abdominal region, which is associated with altered bowel habit or defecation. The underlying mechanism of IBS is not completely understood. IBS seems to be a product of interactions between various factors with genetics, dietary/intestinal microbiota, low-grade inflammation, and stress playing a key role in the pathogenesis of this disease. The crosstalk between the immune system and stress in IBS mechanism is increasingly recognized. Corticotropin-releasing factor (CRF), a major mediator in the stress response, is involved in altered function in GI, including inflammatory processes, colonic transit time, contractile activity, defecation pattern, pain threshold, mucosal secretory function, and barrier functions. This mini review focuses on the recently establish local GI-CRF system, its involvement in modulating the immune response in IBS, and summarizes current IBS animal models and mapping of CRF, CRFR1, and CRFR2 expression in colon tissues. CRF and receptors might be a key molecule involving the immune and movement function via brain–gut axis in IBS.

Highlights

  • Functional gastrointestinal disorders (FGIDs) are a group of idiopathic disorders which affect different parts of the gastrointestinal (GI) tract

  • The FGIDs are classified into six major domains for adults including irritable bowel syndrome (IBS) which is in FGIDs-C

  • This indicates that both central and peripheral Corticotropin-releasing factor (CRF) systems modulate the body response to stress and modulate syndromes that occurs in IBS [11,12,13,14]

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Summary

INTRODUCTION

Functional gastrointestinal disorders (FGIDs) are a group of idiopathic disorders which affect different parts of the gastrointestinal (GI) tract. Animal and human studies have demonstrated that stress stimulates colonic motor function, reflected by decreased-colonic transit time, increased contractile activity, the induction of defecation, and symptoms of diarrhea. CRF, Ucns, and CRF receptors have been identified in myenteric neuron, sensory nerve, sympathetic nerve, enterochromaffin cell, and immune cells in the intestine of animals and human This indicates that both central and peripheral CRF systems modulate the body response to stress and modulate syndromes that occurs in IBS [11,12,13,14]. Recent studies demonstrated a novel therapeutic potential of the mechanisms showing complex interactions between immune cells, epithelial cells, smooth muscle, enteric nerves [28], as well as their respective roles in manifestations of clinical symptoms of FGIDs [29].

Restraint stress for 1 h
Visceral hypersensitivity
Findings
CONCLUSION
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