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Nutr Res Rev. 2016 Jun;29(1):40-59. doi: 10.1017/S0954422416000019. Epub 2016 Apr 18.

Intestinal barrier dysfunction: implications for chronic inflammatory conditions of the bowel.

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1Riddet Institute,Massey University,Private Bag 11-222,Palmerston North,New Zealand.


The intestinal epithelium of adult humans acts as a differentially permeable barrier that separates the potentially harmful contents of the lumen from the underlying tissues. Any dysfunction of this boundary layer that disturbs the homeostatic equilibrium between the internal and external environments may initiate and sustain a biochemical cascade that results in inflammation of the intestine. Key to such dysfunction are genetic, microbial and other environmental factors that, singularly or in combination, result in chronic inflammation that is symptomatic of inflammatory bowel disease (IBD). The aim of the present review is to assess the scientific evidence to support the hypothesis that defective transepithelial transport mechanisms and the heightened absorption of intact antigenic proinflammatory oligopeptides are important contributing factors in the pathogenesis of IBD.


Absorption; CD Crohn’s disease; CeD coeliac disease; Crohn’s disease; EEN exclusive enteral nutrition; EPEC enteropathogenic Escherichia coli; Gastrointestinal tract; IAP intestinal alkaline phosphatase; IBD inflammatory bowel disease; IFN-γ interferon-γ; Immune system; Inflammatory bowel disease; MDP muramyl dipeptide; MMP matrix metalloproteinase; MUC2 mucin 2; Microbiota; NOD nucleotide-binding oligomerisation domain; SIgA secretory IgA; TJ tight junction; TRUC T-bet–/– × Rag2–/–UC; Tri-DAP l-Ala-γ-d-Glu-meso-diaminopimelic acid; UC ulcerative colitis; Ulcerative colitis; fMLP N-formylmethionylleucyl-phenylalanine

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