Abstract

We read with great interest the recent paper published by Zhou et al reporting that upregulation of miR29a in the colonic mucosa of patients with diarrhea-predominant irritable bowel syndrome (IBS-D) is responsible for claudin-1 and nuclear factor-κB-repressing factor reduction leading to increased intestinal permeability.1 These data have been confirmed in miR29-/- mice in both models: water avoidance stress and post-inflammatory colitis. In this paper1, Zhou et al also confirm previous studies showing an increased colonic2 and small intestinal3 permeability in IBS-D patients, with a reduced expression of tight junction proteins, particularly occludin and claudin-1.

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