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Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases
It is now convincingly clear that diet is one of the most influential lifestyle factors contributing to the rise of inflammatory diseases and autoimmunity in both developed and developing countries. In addition, the modern 'Western diet' has changed in recent years with increased caloric i...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4910123/ https://www.ncbi.nlm.nih.gov/pubmed/27350881 http://dx.doi.org/10.1038/cti.2016.29 |
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author | Richards, James L Yap, Yu Anne McLeod, Keiran H Mackay, Charles R Mariño, Eliana |
author_facet | Richards, James L Yap, Yu Anne McLeod, Keiran H Mackay, Charles R Mariño, Eliana |
author_sort | Richards, James L |
collection | PubMed |
description | It is now convincingly clear that diet is one of the most influential lifestyle factors contributing to the rise of inflammatory diseases and autoimmunity in both developed and developing countries. In addition, the modern 'Western diet' has changed in recent years with increased caloric intake, and changes in the relative amounts of dietary components, including lower fibre and higher levels of fat and poor quality of carbohydrates. Diet shapes large-bowel microbial ecology, and this may be highly relevant to human diseases, as changes in the gut microbiota composition are associated with many inflammatory diseases. Recent studies have demonstrated a remarkable role for diet, the gut microbiota and their metabolites—the short-chain fatty acids (SCFAs)—in the pathogenesis of several inflammatory diseases, such as asthma, arthritis, inflammatory bowel disease, colon cancer and wound-healing. This review summarizes how diet, microbiota and gut microbial metabolites (particularly SCFAs) can modulate the progression of inflammatory diseases and autoimmunity, and reveal the molecular mechanisms (metabolite-sensing G protein-coupled receptor (GPCRs) and inhibition of histone deacetylases (HDACs)). Therefore, considerable benefit could be achieved simply through the use of diet, probiotics and metabolites for the prevention and treatment of inflammatory diseases and autoimmunity. |
format | Online Article Text |
id | pubmed-4910123 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49101232016-06-27 Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases Richards, James L Yap, Yu Anne McLeod, Keiran H Mackay, Charles R Mariño, Eliana Clin Transl Immunology Review It is now convincingly clear that diet is one of the most influential lifestyle factors contributing to the rise of inflammatory diseases and autoimmunity in both developed and developing countries. In addition, the modern 'Western diet' has changed in recent years with increased caloric intake, and changes in the relative amounts of dietary components, including lower fibre and higher levels of fat and poor quality of carbohydrates. Diet shapes large-bowel microbial ecology, and this may be highly relevant to human diseases, as changes in the gut microbiota composition are associated with many inflammatory diseases. Recent studies have demonstrated a remarkable role for diet, the gut microbiota and their metabolites—the short-chain fatty acids (SCFAs)—in the pathogenesis of several inflammatory diseases, such as asthma, arthritis, inflammatory bowel disease, colon cancer and wound-healing. This review summarizes how diet, microbiota and gut microbial metabolites (particularly SCFAs) can modulate the progression of inflammatory diseases and autoimmunity, and reveal the molecular mechanisms (metabolite-sensing G protein-coupled receptor (GPCRs) and inhibition of histone deacetylases (HDACs)). Therefore, considerable benefit could be achieved simply through the use of diet, probiotics and metabolites for the prevention and treatment of inflammatory diseases and autoimmunity. Nature Publishing Group 2016-05-13 /pmc/articles/PMC4910123/ /pubmed/27350881 http://dx.doi.org/10.1038/cti.2016.29 Text en Copyright © 2016 Australasian Society for Immunology Inc. http://creativecommons.org/licenses/by-nc-nd/4.0/ 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 | Review Richards, James L Yap, Yu Anne McLeod, Keiran H Mackay, Charles R Mariño, Eliana Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases |
title | Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases |
title_full | Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases |
title_fullStr | Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases |
title_full_unstemmed | Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases |
title_short | Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases |
title_sort | dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4910123/ https://www.ncbi.nlm.nih.gov/pubmed/27350881 http://dx.doi.org/10.1038/cti.2016.29 |
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