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Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection

Clostridioides difficile infection is closely related to the intestinal flora disorders induced by antibiotics, and changes in the intestinal flora may cause the occurrence and development of Clostridioides difficile infection. Epigallocatechin-3-gallate (EGCG) is one of the major bioactive ingredie...

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Autores principales: Wu, Zhengjie, Shen, Jian, Xu, Qiaomai, Xiang, Qiangqiang, Chen, Yunbo, Lv, Longxian, Zheng, Beiwen, Wang, Qiangqiang, Wang, Shuting, Li, Lanjuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9504111/
https://www.ncbi.nlm.nih.gov/pubmed/36145133
http://dx.doi.org/10.3390/nu14183756
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author Wu, Zhengjie
Shen, Jian
Xu, Qiaomai
Xiang, Qiangqiang
Chen, Yunbo
Lv, Longxian
Zheng, Beiwen
Wang, Qiangqiang
Wang, Shuting
Li, Lanjuan
author_facet Wu, Zhengjie
Shen, Jian
Xu, Qiaomai
Xiang, Qiangqiang
Chen, Yunbo
Lv, Longxian
Zheng, Beiwen
Wang, Qiangqiang
Wang, Shuting
Li, Lanjuan
author_sort Wu, Zhengjie
collection PubMed
description Clostridioides difficile infection is closely related to the intestinal flora disorders induced by antibiotics, and changes in the intestinal flora may cause the occurrence and development of Clostridioides difficile infection. Epigallocatechin-3-gallate (EGCG) is one of the major bioactive ingredients of green tea and has been suggested to alleviate the growth of C. difficile in vitro. EGCG can ameliorate several diseases, such as obesity, by regulating the gut microbiota. However, whether EGCG can attenuate C. difficile infection by improving the gut microbiota is unknown. After establishing a mouse model of C. difficile infection, mice were administered EGCG (25 or 50 mg/kg/day) or PBS intragastrically for 2 weeks to assess the benefits of EGCG. Colonic pathology, inflammation, the intestinal barrier, gut microbiota composition, metabolomics, and the transcriptome were evaluated in the different groups. Compared with those of the mice in the CDI group, EGCG improved survival rates after infection, improved inflammatory markers, and restored the damage to the intestinal barrier. Furthermore, EGCG could improve the intestinal microbial community caused by C. difficile infection, such as by reducing the relative abundance of Enterococcaceae and Enterobacteriaceae. Moreover, EGCG can increase short-chain fatty acids, improve amino acid metabolism, and downregulate pathways related to intestinal inflammation. EGCG alters the microbiota and alleviates C. difficile infection, which provides new insights into potential therapies.
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spelling pubmed-95041112022-09-24 Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection Wu, Zhengjie Shen, Jian Xu, Qiaomai Xiang, Qiangqiang Chen, Yunbo Lv, Longxian Zheng, Beiwen Wang, Qiangqiang Wang, Shuting Li, Lanjuan Nutrients Article Clostridioides difficile infection is closely related to the intestinal flora disorders induced by antibiotics, and changes in the intestinal flora may cause the occurrence and development of Clostridioides difficile infection. Epigallocatechin-3-gallate (EGCG) is one of the major bioactive ingredients of green tea and has been suggested to alleviate the growth of C. difficile in vitro. EGCG can ameliorate several diseases, such as obesity, by regulating the gut microbiota. However, whether EGCG can attenuate C. difficile infection by improving the gut microbiota is unknown. After establishing a mouse model of C. difficile infection, mice were administered EGCG (25 or 50 mg/kg/day) or PBS intragastrically for 2 weeks to assess the benefits of EGCG. Colonic pathology, inflammation, the intestinal barrier, gut microbiota composition, metabolomics, and the transcriptome were evaluated in the different groups. Compared with those of the mice in the CDI group, EGCG improved survival rates after infection, improved inflammatory markers, and restored the damage to the intestinal barrier. Furthermore, EGCG could improve the intestinal microbial community caused by C. difficile infection, such as by reducing the relative abundance of Enterococcaceae and Enterobacteriaceae. Moreover, EGCG can increase short-chain fatty acids, improve amino acid metabolism, and downregulate pathways related to intestinal inflammation. EGCG alters the microbiota and alleviates C. difficile infection, which provides new insights into potential therapies. MDPI 2022-09-11 /pmc/articles/PMC9504111/ /pubmed/36145133 http://dx.doi.org/10.3390/nu14183756 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
Wu, Zhengjie
Shen, Jian
Xu, Qiaomai
Xiang, Qiangqiang
Chen, Yunbo
Lv, Longxian
Zheng, Beiwen
Wang, Qiangqiang
Wang, Shuting
Li, Lanjuan
Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection
title Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection
title_full Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection
title_fullStr Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection
title_full_unstemmed Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection
title_short Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection
title_sort epigallocatechin-3-gallate improves intestinal gut microbiota homeostasis and ameliorates clostridioides difficile infection
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9504111/
https://www.ncbi.nlm.nih.gov/pubmed/36145133
http://dx.doi.org/10.3390/nu14183756
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