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The role of immune activation and intestinal permeability in IBS

December's issue of the Alimentary Pharmacology & Therapeutics examines the associations between immune activation, intestinal permeability and the irritable bowel syndrome.

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Irritable bowel syndrome (IBS), one of the most common gastrointestinal disorders, markedly impairing patients' quality of life.

Drug development for IBS treatment has been hampered by the lack of understanding of IBS etiology.

In recent years, numerous data have emerged that suggest the involvement of immune activation in IBS, at least in a subset of patients.

Immune activation was observed more frequently in IBS patients
Alimentary Pharmacology & Therapeutics

Dr Matricon and colleagues from Texas, USA determined whether immune activation and intestinal permeabilisation are more frequently observed in IBS patients compared with healthy controls.
 
The scientific bibliography was searched for irritable bowel syndrome, inflammation, immune activation, permeabilisation, intestine, assay, histology and human.

The retrieved studies, including blood, faecal and histological studies, were analyzed to provide a comprehensive and structured overview of the available data including the type of assay, type of inflammatory marker investigated or intestinal segment studied.
 
The research team observed immune activation more frequently in IBS patients than in healthy controls.

An increase in the number of mast cells and lymphocytes, an alteration in cytokine levels and intestinal permeabilisation were reported in IBS patients.

The researchers found no consistent changes in the numbers of B cells or enterochromaffin cells or in mucosal serotonin production were demonstrated.
 
Dr Matricon's team concludes, "The changes observed were modest and often heterogeneous among the studied population."

"Only appropriate interventions improving irritable bowel syndrome symptoms could highlight and confirm the role of immune activation in this pathophysiology."

Aliment Pharmacol Ther 2012: 36(11pt12): 1009–1031
15 November 2012

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