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Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

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The intestinal epithelial monolayer constitutes a physical and functional barrier between the organism and the external environment. It regulates nutrients absorption, water and ion fluxes, and represents the first defensive barrier against toxins and enteric pathogens. Epithelial cells are linked together at the apical junctional complex by tight junctions that reduce the extracellular space and the passage of charge entities while forming a physical barrier to lipophilic molecules. Cultured intestinal epithelial cells have been extensively used to study intestinal absorption of newly synthesized drugs and the regulation of tight junctions structure and function. In vitro mild irritants, proinflammatory cytokines, toxins and pathogens, and adverse environmental conditions open tight junctions and increase paracellular permeability, an effect often accompanied by immune activation of the enterocytes. Conversely, inhibition of proinflammatory cytokines, exposure to growth factors and probiotics, among others, exert a protective effect. Impaired barrier function results from activation of signalling pathways that lead to alteration of junctional proteins expression and/or distribution. In vivo, intestinal barrier dysfunction is associated with various intestinal and non-intestinal disorders including inflammatory bowel disease, celiac disease, and diarrhoeal infection. This review will describe the current knowledge of the mechanisms regulating tight junctions and intestinal permeability, how these findings have lead to a better understanding of barrier alteration in human intestinal disorders, and what the emerging therapies to treat these pathologies are.

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Keywords: Antigen; Apical Junctional Complex; Barrier dysfunction; Bio-breeding diabetic; E. coli; EPITHELIAL BARRIER; Growth factors; NF-κB; Shigella flex- neri; Vibrio cholera; absorption; actin-myosin cytoskeleton; alcoholic; apoptosis; auto-antibodies; bacteria translocation; bacterial attachment; basolateral factors; calcium depletion; caveolae-vesicles; cellular polarity; cholesterol; colitis; colonic crypt; ctomyosin ring; cytoskeleton; cytoskeleton reorganization; detergent-insoluble; diarrhoea; diffusion; disease; electrical resistance; endogenous factors; endotoxaemia; enterocytes; enteropathies; epithelial injury; epithelial permeability; epithelial resistance; ethanol; exogenous stimuli; exosomes; gastrointestinal; gluten proteins; glycaemia; horseradish peroxidase; hydrophilic molecules; hyperplasia; ileum; immu-noglobulin; immune cells; inflammatory bowel disease; inflammatory bowel syndrome; interferon(; intestinal epithelial cells; intestinal permeability; jejunum; lactulose/mannitol; luminal antigens; macropinocytosis; microdomains; microfilaments; mucosal infiltration; myosin IX; myosin light; myosin light chain kinase; neuro-endocrine; neutrophils; non-intestinal disorders; nonalcoholic; nucleotide; pathogenic strains; pathogens; perijunctional actomyosin ring; phosphoinositide; placebo; polymerization; polymorphisms; polymorphonuclear; pouchitis; predisposition; probiotics; proinflammatory; proinflammatory cytokine; proinflammatory cytokines; protease activated receptor-2; protein kinase; sealing; seru; sphingolipid; subepithelial electrical; sucrase isomaltase; sulfonic acid; tight junction; toxins; transepithelial migration; trypsin-lik; tumour necrosis; ulcerative colitis; xenobiotics; ytoplasmic plaque; zonula occludens toxin

Document Type: Research Article

Publication date: 2011-01-01

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