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Gut microbiota as the key controllers of “healthy” aging of elderly people

Extrinsic factors, such as lifestyle and diet, are shown to be essential in the control of human healthy aging, and thus, longevity. They do so by targeting at least in part the gut microbiome, a collection of commensal microorganisms (microbiota), which colonize the intestinal tract starting after...

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Autores principales: Ragonnaud, Emeline, Biragyn, Arya
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784378/
https://www.ncbi.nlm.nih.gov/pubmed/33397404
http://dx.doi.org/10.1186/s12979-020-00213-w
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author Ragonnaud, Emeline
Biragyn, Arya
author_facet Ragonnaud, Emeline
Biragyn, Arya
author_sort Ragonnaud, Emeline
collection PubMed
description Extrinsic factors, such as lifestyle and diet, are shown to be essential in the control of human healthy aging, and thus, longevity. They do so by targeting at least in part the gut microbiome, a collection of commensal microorganisms (microbiota), which colonize the intestinal tract starting after birth, and is established by the age of three. The composition and abundance of individual microbiota appears to continue to change until adulthood, presumably reflecting lifestyle and geographic, racial, and individual differences. Although most of these changes appear to be harmless, a major shift in their composition in the gut (dysbiosis) can trigger harmful local and systemic inflammation. Recent reports indicate that dysbiosis is increased in aging and that the gut microbiota of elderly people is enriched in pro-inflammatory commensals at the expense of beneficial microbes. The clinical consequence of this change remains confusing due to contradictory reports and a high degree of variability of human microbiota and methodologies used. Here, we present the authors’ thoughts that underscore dysbiosis as a primary cause of aging-associated morbidities, and thus, premature death of elderly people. We provide evidence that the dysbiosis triggers a chain of pathological and inflammatory events. Examples include alteration of levels of microbiota-affected metabolites, impaired function and integrity of the gastrointestinal tract, and increased gut leakiness. All of these enhance systemic inflammation, which when associated with aging is termed inflammaging, and result in consequent aging-associated pathologies.
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spelling pubmed-77843782021-01-14 Gut microbiota as the key controllers of “healthy” aging of elderly people Ragonnaud, Emeline Biragyn, Arya Immun Ageing Review Extrinsic factors, such as lifestyle and diet, are shown to be essential in the control of human healthy aging, and thus, longevity. They do so by targeting at least in part the gut microbiome, a collection of commensal microorganisms (microbiota), which colonize the intestinal tract starting after birth, and is established by the age of three. The composition and abundance of individual microbiota appears to continue to change until adulthood, presumably reflecting lifestyle and geographic, racial, and individual differences. Although most of these changes appear to be harmless, a major shift in their composition in the gut (dysbiosis) can trigger harmful local and systemic inflammation. Recent reports indicate that dysbiosis is increased in aging and that the gut microbiota of elderly people is enriched in pro-inflammatory commensals at the expense of beneficial microbes. The clinical consequence of this change remains confusing due to contradictory reports and a high degree of variability of human microbiota and methodologies used. Here, we present the authors’ thoughts that underscore dysbiosis as a primary cause of aging-associated morbidities, and thus, premature death of elderly people. We provide evidence that the dysbiosis triggers a chain of pathological and inflammatory events. Examples include alteration of levels of microbiota-affected metabolites, impaired function and integrity of the gastrointestinal tract, and increased gut leakiness. All of these enhance systemic inflammation, which when associated with aging is termed inflammaging, and result in consequent aging-associated pathologies. BioMed Central 2021-01-05 /pmc/articles/PMC7784378/ /pubmed/33397404 http://dx.doi.org/10.1186/s12979-020-00213-w Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Ragonnaud, Emeline
Biragyn, Arya
Gut microbiota as the key controllers of “healthy” aging of elderly people
title Gut microbiota as the key controllers of “healthy” aging of elderly people
title_full Gut microbiota as the key controllers of “healthy” aging of elderly people
title_fullStr Gut microbiota as the key controllers of “healthy” aging of elderly people
title_full_unstemmed Gut microbiota as the key controllers of “healthy” aging of elderly people
title_short Gut microbiota as the key controllers of “healthy” aging of elderly people
title_sort gut microbiota as the key controllers of “healthy” aging of elderly people
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784378/
https://www.ncbi.nlm.nih.gov/pubmed/33397404
http://dx.doi.org/10.1186/s12979-020-00213-w
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