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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Mucin2 regulated by Ho1/p38/IL-10 axis plays a protective role in polystyrene nanoplastics-mediated intestinal toxicity.
Mengxing Cui,Qianmei He,Ziwei Wang,Yongjiang Yu,Huan Gao,Ziqi Liu,Honghao Peng,Xue Zhang,Daochuan Li,Liping Chen,Xiumei Xing,Yongmei Xiao,Wen Chen,Qing Wang +13 more
TL;DR: In this paper , the impact of MP/NPs on the intestinal barrier and its mechanism was evaluated using an in-vitro model and invivo model, and it was shown that 20 nm polystyrene nanoplastics (PS-NPs) had higher cytotoxicity than larger particles (200 nm and 2000 nm), and led to an increase of the intestinal permeability along with the decreased expression of tight junction proteins.
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The Crosstalk between Gut Microbiota and Nervous System: A Bidirectional Interaction between Microorganisms and Metabolome
Monica Montagnani,Lucrezia Bottalico,Maria Assunta Potenza,Ioannis Alexandros Charitos,Skender Topi,Marica Colella,Luigi Santacroce +6 more
TL;DR: The role of the intestinal microbiota and the metabolome in the onset and progression of neurological (neurodegenerative, autoimmune) and psychopathological (depression, anxiety disorders, autism) diseases has been explored in this paper .
References
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Microbial translocation is a cause of systemic immune activation in chronic HIV infection
Jason M. Brenchley,David Price,Timothy W. Schacker,Tedi E. Asher,Guido Silvestri,Srinivas S. Rao,Zachary Kazzaz,Ethan Bornstein,Olivier Lambotte,Daniel M. Altmann,Bruce R. Blazar,Benigno Rodriguez,Leia Teixeira-Johnson,Alan L. Landay,Jeffrey N. Martin,Frederick Hecht,Louis J. Picker,Michael M. Lederman,Steven G. Deeks,Daniel C. Douek +19 more
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
Malin E. V. Johansson,Mia Phillipson,Joel Petersson,Anna Velcich,Lena Holm,Gunnar C. Hansson +5 more
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
Li Wen,Ruth E. Ley,Ruth E. Ley,Pavel Volchkov,Peter B. Stranges,Lia Avanesyan,Austin C. Stonebraker,Changyun Hu,F. Susan Wong,Gregory L. Szot,Jeffrey A. Bluestone,Jeffrey I. Gordon,Alexander V. Chervonsky +12 more
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.