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Metagenomic analysis of bile salt biotransformation in the human gut microbiome

BACKGROUND: In the biochemical milieu of human colon, bile acids act as signaling mediators between the host and its gut microbiota. Biotransformation of primary to secondary bile acids have been known to be involved in the immune regulation of human physiology. Several 16S amplicon-based studies wi...

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Autores principales: Das, Promi, Marcišauskas, Simonas, Ji, Boyang, Nielsen, Jens
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6591925/
https://www.ncbi.nlm.nih.gov/pubmed/31234773
http://dx.doi.org/10.1186/s12864-019-5899-3
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author Das, Promi
Marcišauskas, Simonas
Ji, Boyang
Nielsen, Jens
author_facet Das, Promi
Marcišauskas, Simonas
Ji, Boyang
Nielsen, Jens
author_sort Das, Promi
collection PubMed
description BACKGROUND: In the biochemical milieu of human colon, bile acids act as signaling mediators between the host and its gut microbiota. Biotransformation of primary to secondary bile acids have been known to be involved in the immune regulation of human physiology. Several 16S amplicon-based studies with inflammatory bowel disease (IBD) subjects were found to have an association with the level of fecal bile acids. However, a detailed investigation of all the bile salt biotransformation genes in the gut microbiome of healthy and IBD subjects has not been performed. RESULTS: Here, we report a comprehensive analysis of the bile salt biotransformation genes and their distribution at the phyla level. Based on the analysis of shotgun metagenomes, we found that the IBD subjects harbored a significantly lower abundance of these genes compared to the healthy controls. Majority of these genes originated from Firmicutes in comparison to other phyla. From metabolomics data, we found that the IBD subjects were measured with a significantly low level of secondary bile acids and high levels of primary bile acids compared to that of the healthy controls. CONCLUSIONS: Our bioinformatics-driven approach of identifying bile salt biotransformation genes predicts the bile salt biotransformation potential in the gut microbiota of IBD subjects. The functional level of dysbiosis likely contributes to the variation in the bile acid pool. This study sets the stage to envisage potential solutions to modulate the gut microbiome with the objective to restore the bile acid pool in the gut. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12864-019-5899-3) contains supplementary material, which is available to authorized users.
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spelling pubmed-65919252019-07-08 Metagenomic analysis of bile salt biotransformation in the human gut microbiome Das, Promi Marcišauskas, Simonas Ji, Boyang Nielsen, Jens BMC Genomics Research Article BACKGROUND: In the biochemical milieu of human colon, bile acids act as signaling mediators between the host and its gut microbiota. Biotransformation of primary to secondary bile acids have been known to be involved in the immune regulation of human physiology. Several 16S amplicon-based studies with inflammatory bowel disease (IBD) subjects were found to have an association with the level of fecal bile acids. However, a detailed investigation of all the bile salt biotransformation genes in the gut microbiome of healthy and IBD subjects has not been performed. RESULTS: Here, we report a comprehensive analysis of the bile salt biotransformation genes and their distribution at the phyla level. Based on the analysis of shotgun metagenomes, we found that the IBD subjects harbored a significantly lower abundance of these genes compared to the healthy controls. Majority of these genes originated from Firmicutes in comparison to other phyla. From metabolomics data, we found that the IBD subjects were measured with a significantly low level of secondary bile acids and high levels of primary bile acids compared to that of the healthy controls. CONCLUSIONS: Our bioinformatics-driven approach of identifying bile salt biotransformation genes predicts the bile salt biotransformation potential in the gut microbiota of IBD subjects. The functional level of dysbiosis likely contributes to the variation in the bile acid pool. This study sets the stage to envisage potential solutions to modulate the gut microbiome with the objective to restore the bile acid pool in the gut. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12864-019-5899-3) contains supplementary material, which is available to authorized users. BioMed Central 2019-06-25 /pmc/articles/PMC6591925/ /pubmed/31234773 http://dx.doi.org/10.1186/s12864-019-5899-3 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
Das, Promi
Marcišauskas, Simonas
Ji, Boyang
Nielsen, Jens
Metagenomic analysis of bile salt biotransformation in the human gut microbiome
title Metagenomic analysis of bile salt biotransformation in the human gut microbiome
title_full Metagenomic analysis of bile salt biotransformation in the human gut microbiome
title_fullStr Metagenomic analysis of bile salt biotransformation in the human gut microbiome
title_full_unstemmed Metagenomic analysis of bile salt biotransformation in the human gut microbiome
title_short Metagenomic analysis of bile salt biotransformation in the human gut microbiome
title_sort metagenomic analysis of bile salt biotransformation in the human gut microbiome
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6591925/
https://www.ncbi.nlm.nih.gov/pubmed/31234773
http://dx.doi.org/10.1186/s12864-019-5899-3
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