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Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes
This study was designed to explore the different intestinal barrier repair mechanisms of Bifidobacterium breve (B. breve) H4-2 and H9-3 with different exopolysaccharide (EPS) production in mice with colitis. The lipopolysaccharide (LPS)-induced IEC-6 cell inflammation model and dextran sulphate sodi...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9503522/ https://www.ncbi.nlm.nih.gov/pubmed/36145047 http://dx.doi.org/10.3390/nu14183671 |
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author | Niu, Meng-Meng Guo, Huan-Xin Cai, Jun-Wu Meng, Xiang-Chen |
author_facet | Niu, Meng-Meng Guo, Huan-Xin Cai, Jun-Wu Meng, Xiang-Chen |
author_sort | Niu, Meng-Meng |
collection | PubMed |
description | This study was designed to explore the different intestinal barrier repair mechanisms of Bifidobacterium breve (B. breve) H4-2 and H9-3 with different exopolysaccharide (EPS) production in mice with colitis. The lipopolysaccharide (LPS)-induced IEC-6 cell inflammation model and dextran sulphate sodium (DSS)-induced mice colitis model were used. Histopathological changes, epithelial barrier integrity, short-chain fatty acid (SCFA) content, cytokine levels, NF-κB expression level, and intestinal flora were analyzed to evaluate the role of B. breve in alleviating colitis. Cell experiments indicated that both B. breve strains could regulate cytokine levels. In vivo experiments confirmed that oral administration of B. breve H4-2 and B. breve H9-3 significantly increased the expression of mucin, occludin, claudin-1, ZO-1, decreased the levels of IL-6, TNF-α, IL-1β and increased IL-10. Both strains of B. breve also inhibited the expression of the NF-κB signaling pathway. Moreover, B. breve H4-2 and H9-3 intervention significantly increased the levels of SCFAs, reduced the abundance of Proteobacteria and Bacteroidea, and increased the abundance of Muribaculaceae. These results demonstrate that EPS-producing B. breve strains H4-2 and H9-3 can regulate the physical, immune, and microbial barrier to repair the intestinal damage caused by DSS in mice. Of the two strains, H4-2 had a higher EPS output and was more effective at repair than H9-3. These results will provide insights useful for clinical applications and the development of probiotic products for the treatment of colitis. |
format | Online Article Text |
id | pubmed-9503522 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95035222022-09-24 Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes Niu, Meng-Meng Guo, Huan-Xin Cai, Jun-Wu Meng, Xiang-Chen Nutrients Article This study was designed to explore the different intestinal barrier repair mechanisms of Bifidobacterium breve (B. breve) H4-2 and H9-3 with different exopolysaccharide (EPS) production in mice with colitis. The lipopolysaccharide (LPS)-induced IEC-6 cell inflammation model and dextran sulphate sodium (DSS)-induced mice colitis model were used. Histopathological changes, epithelial barrier integrity, short-chain fatty acid (SCFA) content, cytokine levels, NF-κB expression level, and intestinal flora were analyzed to evaluate the role of B. breve in alleviating colitis. Cell experiments indicated that both B. breve strains could regulate cytokine levels. In vivo experiments confirmed that oral administration of B. breve H4-2 and B. breve H9-3 significantly increased the expression of mucin, occludin, claudin-1, ZO-1, decreased the levels of IL-6, TNF-α, IL-1β and increased IL-10. Both strains of B. breve also inhibited the expression of the NF-κB signaling pathway. Moreover, B. breve H4-2 and H9-3 intervention significantly increased the levels of SCFAs, reduced the abundance of Proteobacteria and Bacteroidea, and increased the abundance of Muribaculaceae. These results demonstrate that EPS-producing B. breve strains H4-2 and H9-3 can regulate the physical, immune, and microbial barrier to repair the intestinal damage caused by DSS in mice. Of the two strains, H4-2 had a higher EPS output and was more effective at repair than H9-3. These results will provide insights useful for clinical applications and the development of probiotic products for the treatment of colitis. MDPI 2022-09-06 /pmc/articles/PMC9503522/ /pubmed/36145047 http://dx.doi.org/10.3390/nu14183671 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Niu, Meng-Meng Guo, Huan-Xin Cai, Jun-Wu Meng, Xiang-Chen Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes |
title | Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes |
title_full | Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes |
title_fullStr | Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes |
title_full_unstemmed | Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes |
title_short | Bifidobacterium breve Alleviates DSS-Induced Colitis in Mice by Maintaining the Mucosal and Epithelial Barriers and Modulating Gut Microbes |
title_sort | bifidobacterium breve alleviates dss-induced colitis in mice by maintaining the mucosal and epithelial barriers and modulating gut microbes |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9503522/ https://www.ncbi.nlm.nih.gov/pubmed/36145047 http://dx.doi.org/10.3390/nu14183671 |
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