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.About:
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.read more
Citations
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Journal ArticleDOI
The intestinal epithelial barrier: a therapeutic target?
TL;DR: Mechanisms of intestinal barrier loss and the role of intestinal epithelial barrier function in pathogenesis of both intestinal and systemic diseases are reviewed and a discussion of potential strategies to restore the epithelium is discussed.
Journal ArticleDOI
Leaky gut: mechanisms, measurement and clinical implications in humans.
TL;DR: Clinicians are to discuss the components of the intestinal barrier, the diverse measurements of intestinal permeability, their perturbation in non-inflammatory ‘stressed states’ and the impact of treatment with dietary factors.
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Akkermansia muciniphila-derived extracellular vesicles influence gut permeability through the regulation of tight junctions
Chaithanya Chelakkot,Youngwoo Choi,Dae-Kyum Kim,Hyun Taek Park,Jaewang Ghim,Yonghoon Kwon,Jinseong Jeon,Min-Seon Kim,Young Koo Jee,Yong Song Gho,Hae-Sim Park,Yoon-Keun Kim,Sung H Ryu +12 more
TL;DR: Results imply that AmEVs may act as a functional moiety for controlling gut permeability and that the regulation of intestinal barrier integrity can improve metabolic functions in HFD-fed mice.
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Leaky Gut As a Danger Signal for Autoimmune Diseases
TL;DR: It is hypothesized that modulating the gut microbiota can serve as a potential method for regulating intestinal permeability and may help to alter the course of autoimmune diseases in susceptible individuals.
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The gut microbiome and diet in psychiatry: focus on depression.
TL;DR: Evidence is provided for the gut microbiota as a key factor mediating the link between diet and depressive illness and promise is suggested in the development of interventions targeting the Gut microbiota for the prevention and treatment of common mental health disorders.
References
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Is small intestinal permeability really increased in relatives of patients with Crohn's disease?
TL;DR: Intestinal permeability in relatives was similar to that in the control group, but a subpopulation had abnormally high permeability rates in the absence of clinical evidence for disease, concluding that the original hypothesis is still viable.
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Irritable Bowel Syndrome: Methods, Mechanisms, and Pathophysiology. The confluence of increased permeability, inflammation, and pain in irritable bowel syndrome
TL;DR: The role of the healthy intestinal epithelium as a barrier between the lumen and the rest of the body with a focus on tight junctions is summarized to explore how this increased permeability may elicit immune responses that affect afferent nerves, resulting in the pain associated with IBS.
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Role of the intestinal tight junction modulator zonulin in the pathogenesis of type I diabetes in BB diabetic-prone rats
Tammara L. Watts,Irene Berti,Anna Sapone,Tania Gerarduzzi,Tarcisio Not,Ronald H. Zielke,Alessio Fasano +6 more
TL;DR: Findings suggest that the zonulin-induced loss in small intestinal barrier function is involved in the pathogenesis of T1D in the BB diabetic-prone animal model.
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TNFR2 activates MLCK-dependent tight junction dysregulation to cause apoptosis-mediated barrier loss and experimental colitis.
Liping Su,Liping Su,Sam C. Nalle,Le Shen,Emily S. Turner,Gurminder Singh,Lydia A. Breskin,Ekaterina A. Khramtsova,Galina Khramtsova,Pei-Yun Tsai,Yang Xin Fu,Clara Abraham,Jerrold R. Turner +12 more
TL;DR: In immune-mediated inflammatory bowel disease models, TNFR2 signaling increases long MLCK expression, resulting in tight junction dysregulation, barrier loss, and induction of colitis, which indicates that disease progresses via apoptosis in the absence of M LCK-dependent tight junction regulation.
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Interleukin-10 gene-deficient mice develop a primary intestinal permeability defect in response to enteric microflora.
TL;DR: The data suggest that the intestinal permeability defect in IL-10 gene-deficient mice occurs due to a dysregulated immune response to normal enteric microflora and, furthermore, this permeability defects exists prior to the development of mucosal inflammation.