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Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome

Stress is one of the major causes of irritable bowel syndrome (IBS), which is well-known for perturbing the microbiome and exacerbating IBS-associated symptoms. However, changes in the gut microbiome and metabolome in response to colorectal distention (CRD), combined with restraint stress (RS) admin...

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Autores principales: Hu, Yue, Chen, Fang, Ye, Haiyong, Lu, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8413334/
https://www.ncbi.nlm.nih.gov/pubmed/34475489
http://dx.doi.org/10.1038/s41598-021-97083-z
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author Hu, Yue
Chen, Fang
Ye, Haiyong
Lu, Bin
author_facet Hu, Yue
Chen, Fang
Ye, Haiyong
Lu, Bin
author_sort Hu, Yue
collection PubMed
description Stress is one of the major causes of irritable bowel syndrome (IBS), which is well-known for perturbing the microbiome and exacerbating IBS-associated symptoms. However, changes in the gut microbiome and metabolome in response to colorectal distention (CRD), combined with restraint stress (RS) administration, remains unclear. In this study, CRD and RS stress were used to construct an IBS rat model. The 16S rRNA gene sequencing was used to characterize the microbiota in ileocecal contents. UHPLC-QTOF-MS/MS assay was used to characterize the metabolome of gut microbiota. As a result, significant gut microbial dysbiosis was observed in stress-induced IBS rats, with the obvious enrichment of three and depletion of 11 bacterial taxa in IBS rats, when compared with those in the control group (q < 0.05). Meanwhile, distinct changes in the fecal metabolic phenotype of stress-induced IBS rats were also found, including five increased and 19 decreased metabolites. Furthermore, phenylalanine, tyrosine and tryptophan biosynthesis were the main metabolic pathways induced by IBS stress. Moreover, the altered gut microbiota had a strong correlation with the changes in metabolism of stress-induced IBS rats. Prevotella bacteria are correlated with the metabolism of 1-Naphthol and Arg.Thr. In conclusion, the gut microbiome, metabolome and their interaction were altered. This may be critical for the development of stress-induced IBS.
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spelling pubmed-84133342021-09-07 Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome Hu, Yue Chen, Fang Ye, Haiyong Lu, Bin Sci Rep Article Stress is one of the major causes of irritable bowel syndrome (IBS), which is well-known for perturbing the microbiome and exacerbating IBS-associated symptoms. However, changes in the gut microbiome and metabolome in response to colorectal distention (CRD), combined with restraint stress (RS) administration, remains unclear. In this study, CRD and RS stress were used to construct an IBS rat model. The 16S rRNA gene sequencing was used to characterize the microbiota in ileocecal contents. UHPLC-QTOF-MS/MS assay was used to characterize the metabolome of gut microbiota. As a result, significant gut microbial dysbiosis was observed in stress-induced IBS rats, with the obvious enrichment of three and depletion of 11 bacterial taxa in IBS rats, when compared with those in the control group (q < 0.05). Meanwhile, distinct changes in the fecal metabolic phenotype of stress-induced IBS rats were also found, including five increased and 19 decreased metabolites. Furthermore, phenylalanine, tyrosine and tryptophan biosynthesis were the main metabolic pathways induced by IBS stress. Moreover, the altered gut microbiota had a strong correlation with the changes in metabolism of stress-induced IBS rats. Prevotella bacteria are correlated with the metabolism of 1-Naphthol and Arg.Thr. In conclusion, the gut microbiome, metabolome and their interaction were altered. This may be critical for the development of stress-induced IBS. Nature Publishing Group UK 2021-09-02 /pmc/articles/PMC8413334/ /pubmed/34475489 http://dx.doi.org/10.1038/s41598-021-97083-z Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/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 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/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Hu, Yue
Chen, Fang
Ye, Haiyong
Lu, Bin
Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome
title Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome
title_full Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome
title_fullStr Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome
title_full_unstemmed Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome
title_short Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome
title_sort integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8413334/
https://www.ncbi.nlm.nih.gov/pubmed/34475489
http://dx.doi.org/10.1038/s41598-021-97083-z
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