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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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Journal ArticleDOI

Phosphoproteome Analysis Reveals the Molecular Mechanisms Underlying Deoxynivalenol-Induced Intestinal Toxicity in IPEC-J2 Cells

TL;DR: Identification of relevant signaling pathways yielded new insights into the molecular mechanisms underlying DON-induced intestinal toxicity, and might help in the development of improved mechanism-based risk assessments in animals and humans.
Journal ArticleDOI

Type I IFNs and CD8 T cells increase intestinal barrier permeability after chronic viral infection.

TL;DR: This study demonstrates essential roles for type I IFN signaling and CD8 T cell responses in increasing intestinal permeability during chronic viral infection.
Journal ArticleDOI

Alteration in the mRNA expression of genes associated with gastrointestinal permeability and ileal TNF-α secretion due to the exposure of silver nanoparticles in Sprague–Dawley rats

TL;DR: Interaction of silver with GIT could potentially initiate an inflammatory process that could lead to changes in the gastrointestinal permeability and/or nutrient deficiencies in sex-specific manner.
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Ursodeoxycholic acid inhibits TNFα-induced IL-8 release from monocytes.

TL;DR: UDCA specifically inhibits TNFα-induced IL-8 release from monocytes by inhibiting TRAF2 activation, which would serve to dampen mucosal immune responses in vivo, and support the therapeutic potential of UDCA for IBD.
Book ChapterDOI

Role of Gut Microbiota in Combating Oxidative Stress

TL;DR: Different diseases that induce oxidative stress like pathophysiological, metabolic, neurodegenerative, and microbial infectious diseases and the role of gut microbiota correspondingly to alleviate the toxic state are summarized.
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.
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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.
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.
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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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