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Open AccessJournal ArticleDOI

Mend Your Fences: The Epithelial Barrier and its Relationship With Mucosal Immunity in Inflammatory Bowel Disease

TLDR
This review summarizes the important cellular and molecular barrier components of the intestinal epithelium and emphasizes the mechanisms leading to barrier dysfunction during intestinal inflammation.
Abstract
The intestinal epithelium can be easily disrupted during gut inflammation as seen in inflammatory bowel disease (IBD), such as ulcerative colitis or Crohn's disease. For a long time, research into the pathophysiology of IBD has been focused on immune cell-mediated mechanisms. Recent evidence, however, suggests that the intestinal epithelium might play a major role in the development and perpetuation of IBD. It is now clear that IBD can be triggered by disturbances in epithelial barrier integrity via dysfunctions in intestinal epithelial cell-intrinsic molecular circuits that control the homeostasis, renewal, and repair of intestinal epithelial cells. The intestinal epithelium in the healthy individual represents a semi-permeable physical barrier shielding the interior of the body from invasions of pathogens on the one hand and allowing selective passage of nutrients on the other hand. However, the intestinal epithelium must be considered much more than a simple physical barrier. Instead, the epithelium is a highly dynamic tissue that responds to a plenitude of signals including the intestinal microbiota and signals from the immune system. This epithelial response to these signals regulates barrier function, the composition of the microbiota, and mucosal immune homeostasis within the lamina propria. The epithelium can thus be regarded as a translator between the microbiota and the immune system and aberrant signal transduction between the epithelium and adjacent immune cells might promote immune dysregulation in IBD. This review summarizes the important cellular and molecular barrier components of the intestinal epithelium and emphasizes the mechanisms leading to barrier dysfunction during intestinal inflammation.

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Citations
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Gut microbiota-derived 3-phenylpropionic acid promotes intestinal epithelial barrier function via AhR signaling

TL;DR: In this paper , the authors studied a landscape of the gut microbiome of seven pig breeds using metagenomics and 16S rDNA gene amplicon sequencing and found that Bacteroides fragilis -derived 3-phenylpropionic acid metabolite had an important function on the enhancement of intestinal epithelial barrier.
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Interplay between Serotonin, Immune Response, and Intestinal Dysbiosis in Inflammatory Bowel Disease

TL;DR: In this article , the authors integrated scientific data linking the intestinal microbiota as a regulator of gut serotonin signaling and reuptake, as well as its role in the pathogenesis of IBD.
Journal ArticleDOI

Epithelial Gab1 calibrates RIPK3-dependent necroptosis to prevent intestinal inflammation

TL;DR: In this article , Gab1 deficiency in IECs accounted for the exacerbated colitis induced by dextran sodium sulfate, which irreversibly disrupted the homeostasis of the epithelial barrier and promoted intestinal inflammation.
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A screening model for probiotics against specific metabolic diseases based on caco-2 monolayer membrane

TL;DR: In this article , a Caco-2 cell monolayer membrane model was used to evaluate the effect of 139 Lactobacillus strains on intestinal barrier function in vitro and selected 11 probiotic strains with different regulatory abilities on the gut barrier to determine their effect against osteoporosis or chronic alcoholic liver injury in vivo.
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Cassane diterpenoid ameliorates dextran sulfate sodium-induced experimental colitis by regulating gut microbiota and suppressing tryptophan metabolism

TL;DR: In this article , the authors investigated the bioactivity of caesaldekarin e (CA), a cassane diterpenoid isolated from C. bonduc in their previous work, on dextran sulfate sodium (DSS)-induced experimental colitis and clarified the function mechanism.
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TL;DR: This review, inspired by a spate of recent studies ofdefensins in human diseases and animal models, focuses on the biological function of defensins.
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