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Microbiota dysbiosis and its pathophysiological significance in bowel obstruction

Bowel obstruction (OB) causes local and systemic dysfunctions. Here we investigated whether obstruction leads to alterations in microbiota community composition and total abundance, and if so whether these changes contribute to dysfunctions in OB. Partial colon obstruction was maintained in rats for...

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Autores principales: Hegde, Shrilakshmi, Lin, You-Min, Golovko, George, Khanipov, Kamil, Cong, Yingzi, Savidge, Tor, Fofanov, Yuriy, Shi, Xuan-Zheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6120911/
https://www.ncbi.nlm.nih.gov/pubmed/30177854
http://dx.doi.org/10.1038/s41598-018-31033-0
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author Hegde, Shrilakshmi
Lin, You-Min
Golovko, George
Khanipov, Kamil
Cong, Yingzi
Savidge, Tor
Fofanov, Yuriy
Shi, Xuan-Zheng
author_facet Hegde, Shrilakshmi
Lin, You-Min
Golovko, George
Khanipov, Kamil
Cong, Yingzi
Savidge, Tor
Fofanov, Yuriy
Shi, Xuan-Zheng
author_sort Hegde, Shrilakshmi
collection PubMed
description Bowel obstruction (OB) causes local and systemic dysfunctions. Here we investigated whether obstruction leads to alterations in microbiota community composition and total abundance, and if so whether these changes contribute to dysfunctions in OB. Partial colon obstruction was maintained in rats for 7 days. The mid colon and its intraluminal feces - proximal to the obstruction - were studied. OB did not cause bacterial overgrowth or mucosa inflammation, but induced profound changes in fecal microbiota composition and diversity. At the phylum level, the 16S rRNA sequencing showed a significant decrease in the relative abundance of Firmicutes with corresponding increases in Proteobacteria and Bacteroidetes in OB compared with sham controls. Daily treatment using broad spectrum antibiotics dramatically reduced total bacterial abundance, but increased the relative presence of Proteobacteria. Antibiotics eliminated viable bacteria in the spleen and liver, but not in the mesentery lymph node in OB. Although antibiotic treatment decreased muscle contractility in sham rats, it had little effect on OB-associated suppression of muscle contractility or inflammatory changes in the muscle layer. In conclusion, obstruction leads to marked dysbiosis in the colon. Antibiotic eradication of microbiota had limited effects on obstruction-associated changes in inflammation, motility, or bacterial translocation.
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spelling pubmed-61209112018-09-06 Microbiota dysbiosis and its pathophysiological significance in bowel obstruction Hegde, Shrilakshmi Lin, You-Min Golovko, George Khanipov, Kamil Cong, Yingzi Savidge, Tor Fofanov, Yuriy Shi, Xuan-Zheng Sci Rep Article Bowel obstruction (OB) causes local and systemic dysfunctions. Here we investigated whether obstruction leads to alterations in microbiota community composition and total abundance, and if so whether these changes contribute to dysfunctions in OB. Partial colon obstruction was maintained in rats for 7 days. The mid colon and its intraluminal feces - proximal to the obstruction - were studied. OB did not cause bacterial overgrowth or mucosa inflammation, but induced profound changes in fecal microbiota composition and diversity. At the phylum level, the 16S rRNA sequencing showed a significant decrease in the relative abundance of Firmicutes with corresponding increases in Proteobacteria and Bacteroidetes in OB compared with sham controls. Daily treatment using broad spectrum antibiotics dramatically reduced total bacterial abundance, but increased the relative presence of Proteobacteria. Antibiotics eliminated viable bacteria in the spleen and liver, but not in the mesentery lymph node in OB. Although antibiotic treatment decreased muscle contractility in sham rats, it had little effect on OB-associated suppression of muscle contractility or inflammatory changes in the muscle layer. In conclusion, obstruction leads to marked dysbiosis in the colon. Antibiotic eradication of microbiota had limited effects on obstruction-associated changes in inflammation, motility, or bacterial translocation. Nature Publishing Group UK 2018-09-03 /pmc/articles/PMC6120911/ /pubmed/30177854 http://dx.doi.org/10.1038/s41598-018-31033-0 Text en © The Author(s) 2018 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
Hegde, Shrilakshmi
Lin, You-Min
Golovko, George
Khanipov, Kamil
Cong, Yingzi
Savidge, Tor
Fofanov, Yuriy
Shi, Xuan-Zheng
Microbiota dysbiosis and its pathophysiological significance in bowel obstruction
title Microbiota dysbiosis and its pathophysiological significance in bowel obstruction
title_full Microbiota dysbiosis and its pathophysiological significance in bowel obstruction
title_fullStr Microbiota dysbiosis and its pathophysiological significance in bowel obstruction
title_full_unstemmed Microbiota dysbiosis and its pathophysiological significance in bowel obstruction
title_short Microbiota dysbiosis and its pathophysiological significance in bowel obstruction
title_sort microbiota dysbiosis and its pathophysiological significance in bowel obstruction
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6120911/
https://www.ncbi.nlm.nih.gov/pubmed/30177854
http://dx.doi.org/10.1038/s41598-018-31033-0
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