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Updated: Jul 17, 2026
Functional Assessment of Intestinal Motility and Gut Wall Inflammation in Rodents: Analyses in a Standardized Model of Intestinal Manipulation
Published on: September 11, 2012
Visceral hyperalgesia and intestinal dysmotility in a mouse model of postinfective gut dysfunction
Premysl Bercík1, Lu Wang, Elena F Verdú
1Department of Medicine, McMaster University, Hamilton, Ontario, Canada. bercikp@mcmaster.ca
Background & Aims:
We established the concept that transient enteric infection may lead to persistent gut dysfunction, evident in vitro, in nematode-infected mice. The present study determined whether gut dysfunction in this model involves motor and sensory changes reminiscent of changes found in patients with postinfective irritable bowel syndrome (PI-IBS) and investigated underlying mechanisms.
Methods:
Mice infected up to 70 days previously with Trichinella spiralis (Tsp) underwent videofluoroscopy with image analysis to assess upper gastrointestinal motility. Pseudoaffective responses to colorectal distention (CRD) were assessed using a barostat and validated by single fiber recordings from spinal nerves during CRD. Tissues were examined at different time points for histology, immunohistochemistry, and cytokine analysis. Some mice received dexamethasone intraperitoneally on days 23-25 PI or Tsp antigen orally on days 29, 43, and 57 PI.
Results:
From day 28 PI, no discernible inflammation was present in the gut. Frequency and propagation velocity of intestinal contractions decreased, and retroperistalsis increased at days 28 to 42 PI. CRD induced an allodynic and hyperalgesic response in PI mice, which was accompanied by increased single unit discharge. Gavage of Tsp antigen induced T-cell responses and sustained gut dysfunction for 70 days PI. Administration of dexamethasone postinfection normalized dysmotility and visceral hyperalgesia.
Conclusions:
Long-lasting gut dysmotility and hyperalgesia develop in mice after transient intestinal inflammation. These changes are maintained by luminal exposure to antigen and reversed by corticosteroid treatment. The findings prompt consideration of this as a model of PI-IBS.
Insights
Transient enteric infection can cause long-lasting gut dysfunction, motor, and sensory changes in mice. These symptoms, similar to postinfective irritable bowel syndrome (PI-IBS), were reversed by corticosteroid treatment.
Area of Science:
- Gastroenterology
- Immunology
- Neuroscience
Background:
- Transient enteric infections can lead to persistent gut dysfunction.
- This dysfunction may mimic symptoms seen in postinfective irritable bowel syndrome (PI-IBS).
Purpose of the Study:
- To determine if gut dysfunction in a nematode-infected mouse model involves motor and sensory changes.
- To investigate the underlying mechanisms of these changes.
- To assess if these changes resemble those in patients with PI-IBS.
Main Methods:
- Mice infected with Trichinella spiralis (Tsp) were assessed for upper gastrointestinal motility using videofluoroscopy.
- Visceral sensitivity was evaluated via colorectal distention (CRD) using a barostat and spinal nerve recordings.
- Histology, immunohistochemistry, and cytokine analysis were performed. Dexamethasone or Tsp antigen was administered to some mice.
Main Results:
- No significant gut inflammation was observed from day 28 postinfection (PI).
- PI mice exhibited decreased intestinal contraction frequency and velocity, increased retroperistalsis, and visceral hyperalgesia.
- Tsp antigen exposure sustained gut dysfunction for 70 days PI, which was normalized by dexamethasone treatment.
Conclusions:
- Long-lasting gut dysmotility and hyperalgesia develop after transient intestinal inflammation in mice.
- These changes are sustained by luminal antigen exposure and reversed by corticosteroids.
- This model shows promise for studying PI-IBS.
