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Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia
BACKGROUND: In this study, we aimed to investigate the characteristics of the duodenal mucosal microbiota of patients with intestinal metaplasia (IM) and compare it with those of the gastric mucosal microbiota. METHOD: We collected the duodenal and gastric mucosal samples from 10 adult patients with...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6900849/ https://www.ncbi.nlm.nih.gov/pubmed/31815623 http://dx.doi.org/10.1186/s12866-019-1666-5 |
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author | Gong, Jian Li, Lixiang Zuo, Xiuli Li, Yanqing |
author_facet | Gong, Jian Li, Lixiang Zuo, Xiuli Li, Yanqing |
author_sort | Gong, Jian |
collection | PubMed |
description | BACKGROUND: In this study, we aimed to investigate the characteristics of the duodenal mucosal microbiota of patients with intestinal metaplasia (IM) and compare it with those of the gastric mucosal microbiota. METHOD: We collected the duodenal and gastric mucosal samples from 10 adult patients with IM and 10 healthy controls (HC). The V3-V4 region of the bacterial 16S rRNA gene was examined by high throughput sequencing method. RESULTS: The diversity of the HC duodenal microbiota was higher than that of IM patient based on the Shannon and Simpson index while the Chao indices of IM duodenal mucosal microbiota was significantly higher than that of gastric mucosal microbiota of patients with IM. There was a marked difference in the duodenal microbiota structure between patients with IM and HC (ANOSIM, R = 1, P = 0.001). We also found that the Helicobacter pylori infection in gastric mucosa did not influence the structure of duodenal mucosal microbiota. The gastric mucosal microbiota structure significantly differed between patients with IM and HC who were H. pylori-negative (ANOSIM, R = 0.452, P = 0.042) or H. pylori-positive (ANOSIM, R = 0.548, P = 0.003), respectively. For duodenal mucosal microbiota, genera Lactococcus, Flavobacterium, Psychrobacter, Mysroides, Enhydrobacter, Streptococcus, and Leuconostoc were enriched in patients with IM. In contrast, genera Bacillus, Solibacillus, Lysinibacillus, Exiguobacterium, Oceanobacillus, and Paenibacillus were enriched in HC. CONCLUSION: A marked dysbiosis duodenal mucosal microbiota in patients with IM was observed, and this dysbiosis might be responsible for IM pathogenesis. |
format | Online Article Text |
id | pubmed-6900849 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-69008492019-12-11 Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia Gong, Jian Li, Lixiang Zuo, Xiuli Li, Yanqing BMC Microbiol Research Article BACKGROUND: In this study, we aimed to investigate the characteristics of the duodenal mucosal microbiota of patients with intestinal metaplasia (IM) and compare it with those of the gastric mucosal microbiota. METHOD: We collected the duodenal and gastric mucosal samples from 10 adult patients with IM and 10 healthy controls (HC). The V3-V4 region of the bacterial 16S rRNA gene was examined by high throughput sequencing method. RESULTS: The diversity of the HC duodenal microbiota was higher than that of IM patient based on the Shannon and Simpson index while the Chao indices of IM duodenal mucosal microbiota was significantly higher than that of gastric mucosal microbiota of patients with IM. There was a marked difference in the duodenal microbiota structure between patients with IM and HC (ANOSIM, R = 1, P = 0.001). We also found that the Helicobacter pylori infection in gastric mucosa did not influence the structure of duodenal mucosal microbiota. The gastric mucosal microbiota structure significantly differed between patients with IM and HC who were H. pylori-negative (ANOSIM, R = 0.452, P = 0.042) or H. pylori-positive (ANOSIM, R = 0.548, P = 0.003), respectively. For duodenal mucosal microbiota, genera Lactococcus, Flavobacterium, Psychrobacter, Mysroides, Enhydrobacter, Streptococcus, and Leuconostoc were enriched in patients with IM. In contrast, genera Bacillus, Solibacillus, Lysinibacillus, Exiguobacterium, Oceanobacillus, and Paenibacillus were enriched in HC. CONCLUSION: A marked dysbiosis duodenal mucosal microbiota in patients with IM was observed, and this dysbiosis might be responsible for IM pathogenesis. BioMed Central 2019-12-09 /pmc/articles/PMC6900849/ /pubmed/31815623 http://dx.doi.org/10.1186/s12866-019-1666-5 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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. |
spellingShingle | Research Article Gong, Jian Li, Lixiang Zuo, Xiuli Li, Yanqing Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia |
title | Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia |
title_full | Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia |
title_fullStr | Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia |
title_full_unstemmed | Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia |
title_short | Change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia |
title_sort | change of the duodenal mucosa-associated microbiota is related to intestinal metaplasia |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6900849/ https://www.ncbi.nlm.nih.gov/pubmed/31815623 http://dx.doi.org/10.1186/s12866-019-1666-5 |
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