IBS is a functional GI disorder characterised by abdominal bloating, increased visceral pain perception and an altered defaecation pattern in the absence of an organic cause. The underlying pathophysiological mechanisms that lead to abdominal pain and chronic symptoms in IBS are not fully understood. A common finding is the presence of increased mucosal intestinal permeability and an altered distribution of cell-to-cell adhesion proteins in the intestinal epithelium.1 In particular, patients with diarrhoea-predominant IBS (IBS-D)2 suffer from increased permeability, and this increase correlates with aberrant visceral sensitivity.3 Based on these observations, it is currently hypothesised that impairment of the intestinal barrier integrity facilitates the entrance of food or microbial antigens into the intestinal mucosa, thereby stimulating the mucosal immune system. Accordingly, subsets of patients with IBS show higher numbers and an increased activation of mucosal immunocytes, particularly mast cells. Bioactive mediators released by these...
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