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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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Alanyl-glutamine protects the intestinal barrier function in trained rats against the impact of acute exhaustive exercise.

TL;DR: Exhaustive exercise induced intestinal paracellular leakage associated with the upregulation of claudin-2, a phenomenon protected by AG treatment, and AG partially prevented intestinal training adaptations but also blocked parACEllular leakage during exhaustive exercise involving claud in-2 and occludin gene expression.
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Psychoneuroimmunological approach to gastrointestinal related pain.

TL;DR: By non-invasively modulating the brain-gut axis components such as the psychological and neuroendocrinological status, microbiota, enteric nervous system, or immune cells, a favourable clinical outcome in various chronic gastrointestinal related pain syndromes may be achieved.
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Bacterial translocation in patients undergoing major gastrointestinal surgery and its role in postoperative sepsis

TL;DR: Bacterial translocation in patients undergoing major gastrointestinal surgery and its role in postoperative sepsis was studied in this article, where the authors found that the translocation increased the risk of infection.
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Urolithin A attenuates arsenic-induced gut barrier dysfunction

TL;DR: Treatment with UroA attenuated iAs3+-induced cell toxicity, apoptosis, and oxidative stress in colon epithelial cells and suggest that microbial metabolite, urolithin A (UroA) can potentially be used to protect against environmental hazards by reducing intestinal oxidative stress and by enhancing gut barrier function.
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Estradiol prevented intestinal ischemia and reperfusion-induced changes in intestinal permeability and motility in male rats.

TL;DR: In this paper, the effects of estradiol treatment on local repercussions in an intestinal I/R model were investigated, and the results indicated that the treatment improved intestinal motility, reduced intestinal permeability, and increased mesenteric endothelial nitric oxide synthase and endothelin (ET) protein expression.
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.
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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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