Gut Liver.  2012 Jul;6(3):305-315.

Cellular and Molecular Basis of Intestinal Barrier Dysfunction in the Irritable Bowel Syndrome

  • 1Department of Gastroenterology, Digestive System Research Unit, Hospital Universitari Vall d'Hebron, Institut de Recerca Vall d'Hebron, Universitat Autonoma de Barcelona, Barcelona, Spain.
  • 2Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Barcelona, Spain.


The etiopathogenesis of the irritable bowel syndrome (IBS), one of the most prevalent gastrointestinal disorders, is not well known. The most accepted hypothesis is that IBS is the result of the disturbance of the 'brain-gut axis.' Although the pathophysiological mechanisms of intestinal dysfunction are complex and not completely understood, stress, infections, gut flora, and altered immune response are thought to play a role in IBS development. The intestinal barrier, composed of a single-cell layer, forms a physical barrier that separates the intestinal lumen from the internal milieu. The loss of integrity of this barrier is related with mucosal immune activation and intestinal dysfunction in IBS. The number of mast cells and T lymphocytes is increased in the intestinal mucosa of certain IBS patients, and the mediators released by these cells could compromise the epithelial barrier function and alter nerve signaling within the enteric nervous system. The association of clinical symptoms to structural and functional abnormalities of the mucosal barrier in IBS patients highlights the importance of understanding the physiological role of the gut barrier in the pathogenesis of this disorder. This review summarizes the clinical and experimental evidences indicating the cellular and molecular mechanisms of IBS symptomatology, and its relevance for future translational research.


Intestinal barrier function; Irritable bowel syndrome; Tight junctions; Mast cells

MeSH Terms

Enteric Nervous System
Intestinal Mucosa
Irritable Bowel Syndrome
Mast Cells
Tight Junctions
Translational Medical Research
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