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Updated: Jun 22, 2026
14:09
In vitro Functional Characterization of Mouse Colorectal Afferent Endings
Published on: January 21, 2015
Post-inflammatory modification of colonic afferent mechanosensitivity
P A Hughes1, S M Brierley, L A Blackshaw
1Nerve-Gut Research Laboratory, Department of Gastroenterology and Hepatology, Royal Adelaide Hospital, Adelaide, South Australia, Australia. patrick.hughes@health.sa.gov.au
Clinical and Experimental Pharmacology & Physiology
|July 2, 2009
Summary
Post-infectious irritable bowel syndrome (PI-IBS) involves immune system activation contributing to visceral hypersensitivity. This immune dysregulation, particularly a Type 1 T-helper cell response, appears central to PI-IBS mechanisms.
Area of Science:
- Neurogastroenterology
- Immunology
- Gastroenterology
Background:
- Visceral pain significantly impacts quality of life in irritable bowel syndrome (IBS) patients, often stemming from colonic afferent hypersensitivity.
- Post-infectious IBS (PI-IBS) is linked to preceding gastrointestinal infections, with ongoing immune activation suspected in causing visceral hypersensitivity.
Purpose of the Study:
- To review the interactions between the immune and nervous systems in PI-IBS.
- To explore the role of immune dysregulation in visceral hypersensitivity in PI-IBS.
Main Methods:
- Review of clinical and experimental evidence on immune-nervous system interactions in PI-IBS.
- Examination of immune cell phenotype shifts (e.g., Type 1/Th1 response) and their products in sensitizing colonic afferents.
- Analysis of animal models (trinitrobenzene sulphonic acid-induced colitis) to study Th1-mediated inflammation and biphasic visceral hypersensitivity.
Main Results:
- PI-IBS patients exhibit activated immune systems with a shift towards a Type 1 (Th1-predominating) immune cell phenotype.
- Immune cell products sensitize colonic afferents, contributing to visceral hypersensitivity.
- Animal models demonstrate Th1-mediated inflammation and biphasic visceral hypersensitivity, with delayed hypersensitivity mediated by afferents near blood vessels.
Conclusions:
- Chronic immune system dysregulation is a key mechanism underlying PI-IBS.
- Immune activation and subsequent visceral afferent hypersensitivity are central to the pathophysiology of PI-IBS.
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