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Intestinal permeation and gastrointestinal disease.
J Clin Gastroenterol 2002; 34(4):385-96JC

Abstract

The gastrointestinal tract constitutes one of the largest sites of exposure to the outside environment. The function of the gastrointestinal tract in monitoring and sealing the host interior from intruders is called the gut barrier. A variety of specific and nonspecific mechanisms are in operation to establish the host barrier; these include luminal mechanisms and digestive enzymes, the epithelial cells together with tight junctions in between them, and the gut immune system. Disruptions in the gut barrier follow injury from various causes including nonsteroidal anti-inflammatory drugs and oxidant stress, and involve mechanisms such as adenosine triphosphate depletion and damage to epithelial cell cytoskeletons that regulate tight junctions. Ample evidence links gut barrier dysfunction to multiorgan system failure in sepsis and immune dysregulation. Additionally, contribution of gut barrier dysfunction to gastrointestinal disease is an evolving concept and is the focus of this review. An overview of the evidence for the role of gut barrier dysfunction in disorders such as Crohn's disease, celiac disease, food allergy, acute pancreatitis, non-alcoholic fatty liver disease, and alcoholic liver disease is provided, together with critical insight into the implications of this evidence as a primary disease mechanism.

Authors+Show Affiliations

Division of Gastroenterology and Nutrition, Rush University, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612, USA. mark_t_demeo@rush.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

11907349

Citation

DeMeo, Mark T., et al. "Intestinal Permeation and Gastrointestinal Disease." Journal of Clinical Gastroenterology, vol. 34, no. 4, 2002, pp. 385-96.
DeMeo MT, Mutlu EA, Keshavarzian A, et al. Intestinal permeation and gastrointestinal disease. J Clin Gastroenterol. 2002;34(4):385-96.
DeMeo, M. T., Mutlu, E. A., Keshavarzian, A., & Tobin, M. C. (2002). Intestinal permeation and gastrointestinal disease. Journal of Clinical Gastroenterology, 34(4), pp. 385-96.
DeMeo MT, et al. Intestinal Permeation and Gastrointestinal Disease. J Clin Gastroenterol. 2002;34(4):385-96. PubMed PMID: 11907349.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intestinal permeation and gastrointestinal disease. AU - DeMeo,Mark T, AU - Mutlu,Ece A, AU - Keshavarzian,Ali, AU - Tobin,Mary C, PY - 2002/3/22/pubmed PY - 2002/5/3/medline PY - 2002/3/22/entrez SP - 385 EP - 96 JF - Journal of clinical gastroenterology JO - J. Clin. Gastroenterol. VL - 34 IS - 4 N2 - The gastrointestinal tract constitutes one of the largest sites of exposure to the outside environment. The function of the gastrointestinal tract in monitoring and sealing the host interior from intruders is called the gut barrier. A variety of specific and nonspecific mechanisms are in operation to establish the host barrier; these include luminal mechanisms and digestive enzymes, the epithelial cells together with tight junctions in between them, and the gut immune system. Disruptions in the gut barrier follow injury from various causes including nonsteroidal anti-inflammatory drugs and oxidant stress, and involve mechanisms such as adenosine triphosphate depletion and damage to epithelial cell cytoskeletons that regulate tight junctions. Ample evidence links gut barrier dysfunction to multiorgan system failure in sepsis and immune dysregulation. Additionally, contribution of gut barrier dysfunction to gastrointestinal disease is an evolving concept and is the focus of this review. An overview of the evidence for the role of gut barrier dysfunction in disorders such as Crohn's disease, celiac disease, food allergy, acute pancreatitis, non-alcoholic fatty liver disease, and alcoholic liver disease is provided, together with critical insight into the implications of this evidence as a primary disease mechanism. SN - 0192-0790 UR - https://www.unboundmedicine.com/medline/citation/11907349/full_citation L2 - http://Insights.ovid.com/pubmed?pmid=11907349 DB - PRIME DP - Unbound Medicine ER -