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Rifaximin, Microbiota Biology, and Hepatic Encephalopathy

Rifaximin is beneficial in the treatment of minimal hepatic encephalopathy (MHE). Kang et al. (Clin Transl Gastroenterol 7: e187; doi:10.1038/ctg.2016.44) investigated the effects of rifaximin in a mouse model of MHE-associated microbiota without concomitant liver disease. In addition to some impact...

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Detalles Bibliográficos
Autores principales: Peleman, Cedric, Camilleri, Michael
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5288587/
https://www.ncbi.nlm.nih.gov/pubmed/27711069
http://dx.doi.org/10.1038/ctg.2016.52
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author Peleman, Cedric
Camilleri, Michael
author_facet Peleman, Cedric
Camilleri, Michael
author_sort Peleman, Cedric
collection PubMed
description Rifaximin is beneficial in the treatment of minimal hepatic encephalopathy (MHE). Kang et al. (Clin Transl Gastroenterol 7: e187; doi:10.1038/ctg.2016.44) investigated the effects of rifaximin in a mouse model of MHE-associated microbiota without concomitant liver disease. In addition to some impact on the composition of microbiota, rifaximin altered bacterial functions, ameliorated local and systemic inflammation, and reduced enterocyte glutaminase activity. We discuss these effects as well as the interpretation of the permeability studies, given the potential interaction of dysbiosis with dysfunctional intestinal barrier, leading to systemic inflammation and increased uptake of bacterial metabolites that contribute to MHE in the presence of hepatic dysfunction.
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spelling pubmed-52885872017-02-07 Rifaximin, Microbiota Biology, and Hepatic Encephalopathy Peleman, Cedric Camilleri, Michael Clin Transl Gastroenterol Editorial Rifaximin is beneficial in the treatment of minimal hepatic encephalopathy (MHE). Kang et al. (Clin Transl Gastroenterol 7: e187; doi:10.1038/ctg.2016.44) investigated the effects of rifaximin in a mouse model of MHE-associated microbiota without concomitant liver disease. In addition to some impact on the composition of microbiota, rifaximin altered bacterial functions, ameliorated local and systemic inflammation, and reduced enterocyte glutaminase activity. We discuss these effects as well as the interpretation of the permeability studies, given the potential interaction of dysbiosis with dysfunctional intestinal barrier, leading to systemic inflammation and increased uptake of bacterial metabolites that contribute to MHE in the presence of hepatic dysfunction. Nature Publishing Group 2016-10 2016-10-06 /pmc/articles/PMC5288587/ /pubmed/27711069 http://dx.doi.org/10.1038/ctg.2016.52 Text en Copyright © 2016 The Author(s) http://creativecommons.org/licenses/by-nc-nd/4.0/ Clinical and Translational Gastroenterology is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/
spellingShingle Editorial
Peleman, Cedric
Camilleri, Michael
Rifaximin, Microbiota Biology, and Hepatic Encephalopathy
title Rifaximin, Microbiota Biology, and Hepatic Encephalopathy
title_full Rifaximin, Microbiota Biology, and Hepatic Encephalopathy
title_fullStr Rifaximin, Microbiota Biology, and Hepatic Encephalopathy
title_full_unstemmed Rifaximin, Microbiota Biology, and Hepatic Encephalopathy
title_short Rifaximin, Microbiota Biology, and Hepatic Encephalopathy
title_sort rifaximin, microbiota biology, and hepatic encephalopathy
topic Editorial
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5288587/
https://www.ncbi.nlm.nih.gov/pubmed/27711069
http://dx.doi.org/10.1038/ctg.2016.52
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