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Diet and microbiota in inflammatory bowel disease: The gut in disharmony
Bacterial colonization of the gut shapes both the local and the systemic immune response and is implicated in the modulation of immunity in both healthy and disease states. Recently, quantitative and qualitative changes in the composition of the gut microbiota have been detected in Crohn’s disease a...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Baishideng Publishing Group Inc
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5374124/ https://www.ncbi.nlm.nih.gov/pubmed/28405140 http://dx.doi.org/10.3748/wjg.v23.i12.2124 |
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author | Rapozo, Davy C M Bernardazzi, Claudio de Souza, Heitor Siffert Pereira |
author_facet | Rapozo, Davy C M Bernardazzi, Claudio de Souza, Heitor Siffert Pereira |
author_sort | Rapozo, Davy C M |
collection | PubMed |
description | Bacterial colonization of the gut shapes both the local and the systemic immune response and is implicated in the modulation of immunity in both healthy and disease states. Recently, quantitative and qualitative changes in the composition of the gut microbiota have been detected in Crohn’s disease and ulcerative colitis, reinforcing the hypothesis of dysbiosis as a relevant mechanism underlying inflammatory bowel disease (IBD) pathogenesis. Humans and microbes have co-existed and co-evolved for a long time in a mutually beneficial symbiotic association essential for maintaining homeostasis. However, the microbiome is dynamic, changing with age and in response to environmental modifications. Among such environmental factors, food and alimentary habits, progressively altered in modern societies, appear to be critical modulators of the microbiota, contributing to or co-participating in dysbiosis. In addition, food constituents such as micronutrients are important regulators of mucosal immunity, with direct or indirect effects on the gut microbiota. Moreover, food constituents have recently been shown to modulate epigenetic mechanisms, which can result in increased risk for the development and progression of IBD. Therefore, it is likely that a better understanding of the role of different food components in intestinal homeostasis and the resident microbiota will be essential for unravelling the complex molecular basis of the epigenetic, genetic and environment interactions underlying IBD pathogenesis as well as for offering dietary interventions with minimal side effects. |
format | Online Article Text |
id | pubmed-5374124 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-53741242017-04-12 Diet and microbiota in inflammatory bowel disease: The gut in disharmony Rapozo, Davy C M Bernardazzi, Claudio de Souza, Heitor Siffert Pereira World J Gastroenterol Review Bacterial colonization of the gut shapes both the local and the systemic immune response and is implicated in the modulation of immunity in both healthy and disease states. Recently, quantitative and qualitative changes in the composition of the gut microbiota have been detected in Crohn’s disease and ulcerative colitis, reinforcing the hypothesis of dysbiosis as a relevant mechanism underlying inflammatory bowel disease (IBD) pathogenesis. Humans and microbes have co-existed and co-evolved for a long time in a mutually beneficial symbiotic association essential for maintaining homeostasis. However, the microbiome is dynamic, changing with age and in response to environmental modifications. Among such environmental factors, food and alimentary habits, progressively altered in modern societies, appear to be critical modulators of the microbiota, contributing to or co-participating in dysbiosis. In addition, food constituents such as micronutrients are important regulators of mucosal immunity, with direct or indirect effects on the gut microbiota. Moreover, food constituents have recently been shown to modulate epigenetic mechanisms, which can result in increased risk for the development and progression of IBD. Therefore, it is likely that a better understanding of the role of different food components in intestinal homeostasis and the resident microbiota will be essential for unravelling the complex molecular basis of the epigenetic, genetic and environment interactions underlying IBD pathogenesis as well as for offering dietary interventions with minimal side effects. Baishideng Publishing Group Inc 2017-03-28 2017-03-28 /pmc/articles/PMC5374124/ /pubmed/28405140 http://dx.doi.org/10.3748/wjg.v23.i12.2124 Text en ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Review Rapozo, Davy C M Bernardazzi, Claudio de Souza, Heitor Siffert Pereira Diet and microbiota in inflammatory bowel disease: The gut in disharmony |
title | Diet and microbiota in inflammatory bowel disease: The gut in disharmony |
title_full | Diet and microbiota in inflammatory bowel disease: The gut in disharmony |
title_fullStr | Diet and microbiota in inflammatory bowel disease: The gut in disharmony |
title_full_unstemmed | Diet and microbiota in inflammatory bowel disease: The gut in disharmony |
title_short | Diet and microbiota in inflammatory bowel disease: The gut in disharmony |
title_sort | diet and microbiota in inflammatory bowel disease: the gut in disharmony |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5374124/ https://www.ncbi.nlm.nih.gov/pubmed/28405140 http://dx.doi.org/10.3748/wjg.v23.i12.2124 |
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