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Defining Dysbiosis for a Cluster of Chronic Diseases
The prevalence of many chronic diseases has increased over the last decades. It has been postulated that dysbiosis driven by environmental factors such as antibiotic use is shifting the microbiome in ways that increase inflammation and the onset of chronic disease. Dysbiosis can be defined through t...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733864/ https://www.ncbi.nlm.nih.gov/pubmed/31501492 http://dx.doi.org/10.1038/s41598-019-49452-y |
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author | Wilkins, Lamont J. Monga, Manoj Miller, Aaron W. |
author_facet | Wilkins, Lamont J. Monga, Manoj Miller, Aaron W. |
author_sort | Wilkins, Lamont J. |
collection | PubMed |
description | The prevalence of many chronic diseases has increased over the last decades. It has been postulated that dysbiosis driven by environmental factors such as antibiotic use is shifting the microbiome in ways that increase inflammation and the onset of chronic disease. Dysbiosis can be defined through the loss or gain of bacteria that either promote health or disease, respectively. Here we use multiple independent datasets to determine the nature of dysbiosis for a cluster of chronic diseases that includes urinary stone disease (USD), obesity, diabetes, cardiovascular disease, and kidney disease, which often exist as co-morbidities. For all disease states, individuals exhibited a statistically significant association with antibiotics in the last year compared to healthy counterparts. There was also a statistically significant association between antibiotic use and gut microbiota composition. Furthermore, each disease state was associated with a loss of microbial diversity in the gut. Three genera, Bacteroides, Prevotella, and Ruminococcus, were the most common dysbiotic taxa in terms of being enriched or depleted in disease populations and was driven in part by the diversity of operational taxonomic units (OTUs) within these genera. Results of the cross-sectional analysis suggest that antibiotic-driven loss of microbial diversity may increase the risk for chronic disease. However, longitudinal studies are needed to confirm the causative effect of diversity loss for chronic disease risk. |
format | Online Article Text |
id | pubmed-6733864 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-67338642019-09-20 Defining Dysbiosis for a Cluster of Chronic Diseases Wilkins, Lamont J. Monga, Manoj Miller, Aaron W. Sci Rep Article The prevalence of many chronic diseases has increased over the last decades. It has been postulated that dysbiosis driven by environmental factors such as antibiotic use is shifting the microbiome in ways that increase inflammation and the onset of chronic disease. Dysbiosis can be defined through the loss or gain of bacteria that either promote health or disease, respectively. Here we use multiple independent datasets to determine the nature of dysbiosis for a cluster of chronic diseases that includes urinary stone disease (USD), obesity, diabetes, cardiovascular disease, and kidney disease, which often exist as co-morbidities. For all disease states, individuals exhibited a statistically significant association with antibiotics in the last year compared to healthy counterparts. There was also a statistically significant association between antibiotic use and gut microbiota composition. Furthermore, each disease state was associated with a loss of microbial diversity in the gut. Three genera, Bacteroides, Prevotella, and Ruminococcus, were the most common dysbiotic taxa in terms of being enriched or depleted in disease populations and was driven in part by the diversity of operational taxonomic units (OTUs) within these genera. Results of the cross-sectional analysis suggest that antibiotic-driven loss of microbial diversity may increase the risk for chronic disease. However, longitudinal studies are needed to confirm the causative effect of diversity loss for chronic disease risk. Nature Publishing Group UK 2019-09-09 /pmc/articles/PMC6733864/ /pubmed/31501492 http://dx.doi.org/10.1038/s41598-019-49452-y Text en © The Author(s) 2019 Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Wilkins, Lamont J. Monga, Manoj Miller, Aaron W. Defining Dysbiosis for a Cluster of Chronic Diseases |
title | Defining Dysbiosis for a Cluster of Chronic Diseases |
title_full | Defining Dysbiosis for a Cluster of Chronic Diseases |
title_fullStr | Defining Dysbiosis for a Cluster of Chronic Diseases |
title_full_unstemmed | Defining Dysbiosis for a Cluster of Chronic Diseases |
title_short | Defining Dysbiosis for a Cluster of Chronic Diseases |
title_sort | defining dysbiosis for a cluster of chronic diseases |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733864/ https://www.ncbi.nlm.nih.gov/pubmed/31501492 http://dx.doi.org/10.1038/s41598-019-49452-y |
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