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Being the most prevalent gastrointestinal disorder, the irritable bowel syndrome (IBS) remains as major challenge for the biomedical community due to its unclear pathophysiology, the lack of effective therapeutic options, and its negative impact on a sufferer’s quality of life. Not yet identified as a cause or a consequence, abnormal intestinal permeability characterises chronic inflammatory disorders such as coeliac disease, inflammatory bowel disease, multiple sclerosis or diabetes, in which this phenomenon has been connected to the disappearance of key structural proteins of the intestinal epithelial barrier.1 Oddly enough, although altered intestinal permeability has also been reported in patients with IBS, and the grade of barrier defect related to the onset of symptoms,2 the mechanism responsible and the mediators are ignored. It is therefore of great importance to perform studies to unravel the underlying events, and ultimately design and develop improved diagnostic and therapeutic tools. In this respect, the study by Piche and colleague3 in this issue of Gut (see page 195) represents a significant contribution to this endeavour.
IBS is still quoted as an archetype for functional digestive disorders. The truth is that this time-honoured truism should be revised based on mounting evidence for a low-grade inflammatory process as a plausible contributor to IBS manifestations, at least in some subtypes.4 Mucosal inflammation has been described throughout the gut, from the jejunum to the rectum, and includes the proliferation of various lamina propria immune cells, mostly CD3+/CD8+/CD25+ lymphocytes, tryptase/CD117+ mast cells, and endocrine cells.5 This cellular infiltrate is commonly paralleled by the subtle increase of para-inflammatory molecules or their genes (interleukin 1β (IL1β), tumour necrosis factor α (TNFα), IL6, IL6r, transforming growth factor β (TGFβ), IL10, tryptase) in the mucosa, luminal content and peripheral circulation as well.6 7 Whether …