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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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Phaseolus vulgaris extract ameliorates high-fat diet-induced colonic barrier dysfunction and inflammation in mice by regulating peroxisome proliferator-activated receptor expression and butyrate levels

TL;DR: It is shown that prolonged treatment with PHAS significantly reduces some pathological features related to the metabolic syndrome-like condition, such as inflammation and intestinal barrier disruption; therefore, PHAS could be a valid tool to be associated with the therapeutic strategy.
Journal ArticleDOI

Ameliorative effect of graphene nanosheets against arsenic-induced toxicity in mice by oral exposure

TL;DR: In this article, the authors investigated the effects of graphene on arsenic-induced toxicity by oral exposure in mice and found that the addition of graphene significantly reduced the toxicity of arsenic in the intestine and liver of mice, and the high-concentration graphene exhibited greater toxicity reduction effects.
Journal ArticleDOI

Astrovirus-induced epithelial-mesenchymal transition via activated TGF-β increases viral replication

TL;DR: It is demonstrated that HAstV replication induces epithelial-mesenchymal transition (EMT), by upregulating the transcription of EMT-related genes within 8 hours post-infection, followed by the loss of cell-cell contacts and disruption of polarity by 24 hpi.
Book ChapterDOI

Establishment of Intestinal Epithelial Cell Monolayers and Their Use in Calcium Switch Assay for Assessment of Intestinal Tight Junction Assembly.

TL;DR: In this article, a stepwise protocol for culture of intestinal epithelial cell monolayers using T84 cell line as an in vitro model and the Ca2+-switch assay for evaluating tight junction assembly was provided.
References
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Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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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