The intestinal epithelium is a single-cell layer that constitutes the largest and most important barrier against the external environment. It acts as a selectively permeable barrier, permitting the absorption of nutrients, electrolytes, and water while maintaining an effective defense against intraluminal toxins, antigens, and enteric flora. The epithelium maintains its selective barrier function through the formation of complex protein-protein networks that mechanically link adjacent cells and seal the intercellular space. The protein networks connecting epithelial cells form 3 adhesive complexes: desmosomes, adherens junctions, and tight junctions. These complexes consist of transmembrane proteins that interact extracellularly with adjacent cells and intracellularly with adaptor proteins that link to the cytoskeleton. Over the past decade, there has been increasing recognition of an association between disrupted intestinal barrier function and the development of autoimmune and inflammatory diseases. In this review we summarize the evolving understanding of the molecular composition and regulation of intestinal barrier function. We discuss the interactions between innate and adaptive immunity and intestinal epithelial barrier function, as well as the effect of exogenous factors on intestinal barrier function. Finally, we summarize clinical and experimental evidence demonstrating intestinal epithelial barrier dysfunction as a major factor contributing to the predisposition to inflammatory diseases, including food allergy, inflammatory bowel diseases, and celiac disease.
"Other enteric changes associated with stress include gut motility, permeability , and alterations to ion, fluid, and mucus secretion (Alverdy and Aoys, 1991; Karavolos et al., 2008). These changes have been linked to mast cells which are important effectors of the brain-gut axis and translate stress signals into the release of a wide range of neurotransmitters and pro-inflammatory cytokines, with dramatic effects on gastrointestinal physiology (Groschwitz and Hogan, 2009; Bailey et al., 2011; Lamprecht and Frauwallner, 2012). Studies have shown that dexamethasone can modulate enteric tight junction integrity in mammary tissue and also at the blood-brain barrier, but reports regarding gastrointestinal tight junctions are rare (Boivin et al., 2007; Tenenbaum et al., 2008). "
"Signaling through the zonulin receptor causes remodeling of the cytoskeleton and down-regulation of ZO-1 and occludin . This disassembly of the tight junctions results in enhanced gut permeability  . The detrimental effect of zonulin on the gut barrier function was confirmed by Watts and coworkers. "
"Intestinal epithelial cells (IECs) participating in mucosal barrier function are conventional enterocytes, goblet cells, entero-endocrine cells and Paneth cells. The luminal secretion of mucins and non-specific antimicrobial peptides by goblet cells and Paneth cells, respectively, establishes a physical and biochemical barrier to microbial contact with the epithelial surface and underlying immune cells  . The mucosal barriers (membrane and mucus) provide the first line of defense and directly communicate with microbiota in the gut . "
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