Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation

Abstract Clostridioides difficile infection (CDI) represents the leading cause of nosocomial diarrhea worldwide and is associated with gut dysbiosis and intestinal damage. Clostridium butyricum MIYAIRI 588 (CBM 588) contributes significantly to reduce epithelial damage. However, the impacts of CBM 5...

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Autores principales:	Mao Hagihara, Tadashi Ariyoshi, Yasutoshi Kuroki, Shuhei Eguchi, Seiya Higashi, Takeshi Mori, Tsunemasa Nonogaki, Kenta Iwasaki, Makoto Yamashita, Nobuhiro Asai, Yusuke Koizumi, Kentaro Oka, Motomichi Takahashi, Yuka Yamagishi, Hiroshige Mikamo
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/367a9a03f9654d4f92dbc8e0bc0239a9
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spelling	oai:doaj.org-article:367a9a03f9654d4f92dbc8e0bc0239a92021-12-02T17:55:13ZClostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation10.1038/s41598-021-94572-z2045-2322https://doaj.org/article/367a9a03f9654d4f92dbc8e0bc0239a92021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94572-zhttps://doaj.org/toc/2045-2322Abstract Clostridioides difficile infection (CDI) represents the leading cause of nosocomial diarrhea worldwide and is associated with gut dysbiosis and intestinal damage. Clostridium butyricum MIYAIRI 588 (CBM 588) contributes significantly to reduce epithelial damage. However, the impacts of CBM 588 on antibacterial therapy for CDI are not clear. Here we show that CBM 588 enhanced the antibacterial activity of fidaxomicin against C. difficile and negatively modulated gut succinate levels to prevent C. difficile proliferation and downregulate tumor necrosis factor-α (TNF-α) producing macrophages in the colon lumina propria (cLP), resulting in a significant decrease in colon epithelial damage. Additionally, CBM 588 upregulated T cell-dependent pathogen specific immunoglobulin A (IgA) via interleukin (IL)-17A producing CD4+ cells and plasma B cells in the cLP, and Th17 cells in the cLP enhanced the gut epithelial barrier function. IL-17A and succinic acid modulations with CBM 588 enhance gut colonization resistance to C. difficile and protect the colon tissue from CDI.Mao HagiharaTadashi AriyoshiYasutoshi KurokiShuhei EguchiSeiya HigashiTakeshi MoriTsunemasa NonogakiKenta IwasakiMakoto YamashitaNobuhiro AsaiYusuke KoizumiKentaro OkaMotomichi TakahashiYuka YamagishiHiroshige MikamoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Mao Hagihara Tadashi Ariyoshi Yasutoshi Kuroki Shuhei Eguchi Seiya Higashi Takeshi Mori Tsunemasa Nonogaki Kenta Iwasaki Makoto Yamashita Nobuhiro Asai Yusuke Koizumi Kentaro Oka Motomichi Takahashi Yuka Yamagishi Hiroshige Mikamo Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation
description	Abstract Clostridioides difficile infection (CDI) represents the leading cause of nosocomial diarrhea worldwide and is associated with gut dysbiosis and intestinal damage. Clostridium butyricum MIYAIRI 588 (CBM 588) contributes significantly to reduce epithelial damage. However, the impacts of CBM 588 on antibacterial therapy for CDI are not clear. Here we show that CBM 588 enhanced the antibacterial activity of fidaxomicin against C. difficile and negatively modulated gut succinate levels to prevent C. difficile proliferation and downregulate tumor necrosis factor-α (TNF-α) producing macrophages in the colon lumina propria (cLP), resulting in a significant decrease in colon epithelial damage. Additionally, CBM 588 upregulated T cell-dependent pathogen specific immunoglobulin A (IgA) via interleukin (IL)-17A producing CD4+ cells and plasma B cells in the cLP, and Th17 cells in the cLP enhanced the gut epithelial barrier function. IL-17A and succinic acid modulations with CBM 588 enhance gut colonization resistance to C. difficile and protect the colon tissue from CDI.
format	article
author	Mao Hagihara Tadashi Ariyoshi Yasutoshi Kuroki Shuhei Eguchi Seiya Higashi Takeshi Mori Tsunemasa Nonogaki Kenta Iwasaki Makoto Yamashita Nobuhiro Asai Yusuke Koizumi Kentaro Oka Motomichi Takahashi Yuka Yamagishi Hiroshige Mikamo
author_facet	Mao Hagihara Tadashi Ariyoshi Yasutoshi Kuroki Shuhei Eguchi Seiya Higashi Takeshi Mori Tsunemasa Nonogaki Kenta Iwasaki Makoto Yamashita Nobuhiro Asai Yusuke Koizumi Kentaro Oka Motomichi Takahashi Yuka Yamagishi Hiroshige Mikamo
author_sort	Mao Hagihara
title	Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation
title_short	Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation
title_full	Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation
title_fullStr	Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation
title_full_unstemmed	Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation
title_sort	clostridium butyricum enhances colonization resistance against clostridioides difficile by metabolic and immune modulation
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/367a9a03f9654d4f92dbc8e0bc0239a9
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Clostridium butyricum enhances colonization resistance against Clostridioides difficile by metabolic and immune modulation

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