title: Intestinal Permeability in Inflammatory Bowel Disease: Pathogenesis, Clinical Evaluation, and Therapy of Leaky Gut.
abstract: The pathogenesis of inflammatory bowel disease (IBD) is multifactorial with data suggesting the role of a disturbed interaction between the gut and the intestinal microbiota. A defective mucosal barrier may result in increased intestinal permeability which promotes the exposition to luminal content and triggers an immunological response that promotes intestinal inflammation. IBD patients display several defects in the many specialized components of mucosal barrier, from the mucus layer composition to the adhesion molecules that regulate paracellular permeability. These alterations may represent a primary dysfunction in Crohn's disease, but they may also perpetuate chronic mucosal inflammation in ulcerative colitis. In clinical practice, several studies have documented that changes in intestinal permeability can predict IBD course. Functional tests, such as the sugar absorption tests or the novel imaging technique using confocal laser endomicroscopy, allow an in vivo assessment of gut barrier integrity. Antitumor necrosis factor-α (TNF-α) therapy reduces mucosal inflammation and restores intestinal permeability in IBD patients. Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further studies are needed before considering permeability manipulation as a therapeutic target in IBD.
authors.affiliation: Department of Surgical, Oncological and Gastroenterological Sciences, University of Padua, 35128 Padova, Italy.
authors.forename: Andrea
authors.initials: A
authors.lastname: Michielan
authors.affiliation: Department of Surgical, Oncological and Gastroenterological Sciences, University of Padua, 35128 Padova, Italy.
authors.forename: Renata
authors.initials: R
authors.lastname: D'Incà
mesh_terms: D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D010539:Permeability; D019936:Probiotics / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D015032:Zinc / Q000627:therapeutic use
chemical_list: D014409:Tumor Necrosis Factor-alpha; D015032:Zinc