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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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Citations
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Bidirectional association between fibromyalgia and gastroesophageal reflux disease: two population-based retrospective cohort analysis.

TL;DR: Fibromyalgia (FM) tends to coexist with gastroesophageal reflux disease (GERD) and the present study suggests a bidirectional relationship between FM and GERD, with a greater risk of developing GERD for patients with FM than developing FM for Patients with GERD.
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Filtered Kombucha tea ameliorates the leaky gut syndrome in young and old mice model of colitis.

TL;DR: The results suggest KT as a promising therapeutic candidate to reduce intestinal permeability and healing effect of Kombucha tea on the gastrointestinal system, particularly its extraordinary healing effects on intestinal ulcers has been purported traditionally and rarely reported scientifically.
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The interplay between gut microbiota and autism spectrum disorders: A focus on immunological pathways.

TL;DR: An overview of how gut microbes and their metabolites are associated with neurobehavioral features of ASD through various immunologic mechanisms is provided and the potential therapeutic options that could modify these features are discussed.
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Checkpoint Kinase 1 Activation Enhances Intestinal Epithelial Barrier Function via Regulation of Claudin-5 Expression

TL;DR: The results suggest that Chk1 activation by daunorubicin and rebeccamycin induced claudin-5 expression and enhanced TJ barrier function in Caco-2 cell monolayer, which suggests a link between DNA damage and TJ integrity in the human intestine.
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Probing endocytosis from the enterocyte brush border using fluorescent lipophilic dyes: lipid sorting at the apical cell surface.

TL;DR: Lipid sorting by selective endocytosis therefore may be a process in the enterocytes aimed to generate and maintain a unique lipid composition in the brush border prior to internalization.
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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