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Serotonin, inflammation, and IBS: fitting the jigsaw together?
1Department of Gastroenterology, Wolfson Digestive Diseases Centre, Nottingham, UK. robin.spiller@nottingham.ac.uk
Journal of Pediatric Gastroenterology and Nutrition
|February 7, 2008
Summary
Postinfective irritable bowel syndrome (IBS) can develop after infections, with severe diarrhea being a key risk factor. Serotonin release patterns and low-grade inflammation may play roles in IBS development and symptoms.
Area of Science:
- Gastroenterology
- Immunology
- Neurogastroenterology
Background:
- Unexplained diarrhea frequently leads to gastroenterologic referral, with Irritable Bowel Syndrome (IBS) being a common diagnosis.
- A subset of IBS patients report symptom onset after infective gastroenteritis, termed postinfective IBS.
- Postinfective IBS affects 7-31% of infected individuals and is a nonspecific response to injury.
Purpose of the Study:
- To explore risk factors and underlying mechanisms of postinfective IBS.
- To investigate the role of serotonin release and low-grade inflammation in IBS pathogenesis.
Main Methods:
- Review of risk factors including illness severity, bacterial toxigenicity, age, sex, and psychological factors.
- Analysis of rectal biopsies for enteroendocrine cell and lymphocyte counts.
- Examination of postprandial serotonin release in IBS subtypes and correlation with inflammation.
Main Results:
- Severity of initial diarrhea is the strongest risk factor for postinfective IBS; bacterial factors, age, and sex are also significant.
- Increased enteroendocrine cells and lymphocytes in rectal biopsies are associated with IBS.
- Both postinfective IBS and IBS with diarrhea show increased postprandial serotonin release, while constipation-predominant IBS shows decreased release.
Conclusions:
- Postinfective IBS shares pathophysiological mechanisms with other IBS subtypes, particularly involving serotonin dysregulation.
- Low-grade inflammation may be present in IBS with diarrhea, but reliable predictive markers are needed.
- Further research is required to identify inflammatory markers for targeted therapies in IBS.
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