Microbe-host interactions in post-infectious irritable bowel syndrome (PI-IBS)

In the Western world Irritable bowel syndrome (IBS) affects approximately one in five. The disease involves abdominal pain, bloating, diarrhoea and/or constipation symptoms. Today the underlying pathogenesis of IBS is unknown. Subsets of IBS patients develop the disease following an infection of the gastrointestinal tract and this has led to the hypothesis that the initial infection disturbs the balance of the patient's immune system and the naturally occurring bacteria in the gut.

The PI-IBS patients in our study show an increased number of lamina propria lymphocytes in the gut. B- and T-lymphocyte pattern in the lamina propria of PI-IBS patients is altered in comparison to healthy controls and display more active lymphocyte.

In the same group of PI-IBS patients the microbiota composition in both faecal and biopsies are altered compared to healthy controls. The bacteria in the intestine have many immune-regulatory functions. Commensal bacteria stabilize the epithelial barrier between the lumen of the gut and the body tissues and stimulate regulatory T cells in the lamina propria.

Specific bacteria and lymphocytes interaction affects cytokine production and translation of immune regulatory molecules. We aim to study how an aberrant interaction may lead to the A change in the leakage of the epithelium could be an explanation for why we see an altered immune response in the lamina propria, and therefore we will investigate whether permeability may have increased because out of an altered expression of the proteins that binds the epithelial cells.

Our goal with this project is to find causes of PI-IBS and thereby promote the development of preventive and curative measures for the patients affected by the disease.