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Open AccessJournal ArticleDOI

Intestinal Permeability Defects: Is It Time to Treat?

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TLDR
The correlation between increased intestinal permeability and disease has caught the attention of the public, leading to a rise in popularity of the diagnosis of "leaky gut syndrome," which encompasses a range of systemic disorders.
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This article is published in Clinical Gastroenterology and Hepatology.The article was published on 2013-09-01 and is currently open access. It has received 268 citations till now. The article focuses on the topics: Intestinal mucosa & Intestinal permeability.

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Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability.

TL;DR: In this paper, Baicalin (BA) extracts from the root of Scutellaria baicalensis were extracted from HT-29 cells and they were exposed to lipopolysaccharide (LPS), in presence or absence of BA, for 4 hours.
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Glycine supplementation to breast-fed piglets attenuates post-weaning jejunal epithelial apoptosis: a functional role of CHOP signaling.

TL;DR: Results indicated that preweaning glycine supplementation improved the intestinal development of post-weaning piglets and was associated with improved intestinal mucosal barrier and reduced apoptosis of enterocytes through CHOP signaling.
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Mechanism of intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease: An observational study.

TL;DR: Dysfunctional and structural changes were observed in the intestinal mucosal barrier in COPD model rats, which may be associated with the increased intestinal inflammatory responses.
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The role of IgG hypersensitivity in the pathogenesis and therapy of depressive disorders

TL;DR: A new hypothesis connecting the inflammatory theory of depression with IgG food hypersensitivity and leaky gut syndrome is presented, suggesting a new potential pathway that may mediate the pathogenesis of depression implies the existence of subsequent developmental stages.
References
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Microbial translocation is a cause of systemic immune activation in chronic HIV infection

TL;DR: It is shown that increased lipopolysaccharide is bioactive in vivo and correlates with measures of innate and adaptive immune activation, which establish a mechanism for chronic immune activation in the context of a compromised gastrointestinal mucosal surface and provide new directions for therapeutic interventions that modify the consequences of acute HIV infection.
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Intestinal mucosal barrier function in health and disease.

TL;DR: Recent advances have uncovered mechanisms by which the intestinal mucosal barrier is regulated in response to physiological and immunological stimuli, along with evidence that this regulation shapes mucosal immune responses in the gut and, when dysfunctional, may contribute to disease.
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Microbial translocation is a cause of systemic immune activation in chronic HIV infection

TL;DR: It is shown that circulating microbial products, probably derived from the gastrointestinal tract, are a cause of HIV-related systemic immune activation and increased lipopolysaccharide is bioactive in vivo and correlates with measures of innate and adaptive immune activation.
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The inner of the two Muc2 mucin-dependent mucus layers in colon is devoid of bacteria

TL;DR: Findings show that the Muc2 mucin can build a mucus barrier that separates bacteria from the colon epithelia and suggest that defects in this mucus can cause colon inflammation.
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Innate immunity and intestinal microbiota in the development of Type 1 diabetes

TL;DR: It is found that MyD88 deficiency changes the composition of the distal gut microbiota, and that exposure to the microbiota of specific pathogen-free MyD 88-negative NOD donors attenuates T1D in germ-free NOD recipients.
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