Introduction

The main task of the gastrointestinal system is to digest food and absorb nutrients, while preventing systemic dissemination of pathogens and limiting the diffusion of commensal microorganisms. To facilitate these functions, the digestive tract is lined with a highly dynamic and specialised structure known as the intestinal epithelial barrier (IEB), which consists of a monolayer of epithelial cells in association with goblet cells, enterochromaffin cells and Paneth cells.1 Due to the presence of serrated tight junctions, mucus layer and the secreted antimicrobial molecules, the IEB acts as an essential line of defence to shield the deeper tissues from the external environment, avoiding colonisation of harmful agents.1 Alterations in the IEB leading to increased intestinal permeability are indeed observed in a wide range of gastrointestinal diseases, such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), caeliac disease and enteric infections.1 Whether deregulation of the IEB is an initial detrimental step perturbing intestinal homeostasis or rather a consequence of an established pathology is still a matter of controversial but interesting debate.