Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice

Intracerebral hemorrhage (ICH) induces a strong hematoma-related neuroinflammatory reaction and alters peripheral immune homeostasis. Recent research has found that gut microbiota plays a role in neurodegeneration and autoimmune diseases by regulating immune homeostasis and neuroinflammation. Theref...
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Autor*in:	Xiaobo Yu [verfasserIn] Guoyang Zhou [verfasserIn] Bo Shao [verfasserIn] Hang Zhou [verfasserIn] Chaoran Xu [verfasserIn] Feng Yan [verfasserIn] Lin Wang [verfasserIn] Gao Chen [verfasserIn] Jianru Li [verfasserIn] Xiongjie Fu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	intracerebral hemorrhage neuroinflammation gut microbiota dysbiosis T cell

Übergeordnetes Werk:	In: Frontiers in Microbiology - Frontiers Media S.A., 2011, 12(2021)
Übergeordnetes Werk:	volume:12 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fmicb.2021.647304

Katalog-ID:	DOAJ053209427

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520			\|a Intracerebral hemorrhage (ICH) induces a strong hematoma-related neuroinflammatory reaction and alters peripheral immune homeostasis. Recent research has found that gut microbiota plays a role in neurodegeneration and autoimmune diseases by regulating immune homeostasis and neuroinflammation. Therefore, we investigated the relationship between ICH, microbiota alteration, and immune responses after hematoma-induced acute brain injury. In our study, we used a mouse model of ICH, and 16S ribosomal RNA sequencing showed that ICH causes gut microbiota dysbiosis, which in turn affects ICH outcome through immune-mediated mechanisms. There was prominent reduced species diversity and microbiota overgrowth in the dysbiosis induced by ICH, which may reduce intestinal motility and increase gut permeability. In addition, recolonizing ICH mice with a normal health microbiota ameliorates functional deficits and neuroinflammation after ICH. Meanwhile, cell-tracking studies have demonstrated the migration of intestinal lymphocytes to the brain after ICH. In addition, therapeutic transplantation of fecal microbiota improves intestinal barrier damage. These results support the conclusion that the gut microbiome is a target of ICH-induced systemic alteration and is considered to have a substantial impact on ICH outcome.
650		4	\|a intracerebral hemorrhage
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spelling	10.3389/fmicb.2021.647304 doi (DE-627)DOAJ053209427 (DE-599)DOAJ28b00b28516945f1b17a35222f4ec77c DE-627 ger DE-627 rakwb eng QR1-502 Xiaobo Yu verfasserin aut Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Intracerebral hemorrhage (ICH) induces a strong hematoma-related neuroinflammatory reaction and alters peripheral immune homeostasis. Recent research has found that gut microbiota plays a role in neurodegeneration and autoimmune diseases by regulating immune homeostasis and neuroinflammation. Therefore, we investigated the relationship between ICH, microbiota alteration, and immune responses after hematoma-induced acute brain injury. In our study, we used a mouse model of ICH, and 16S ribosomal RNA sequencing showed that ICH causes gut microbiota dysbiosis, which in turn affects ICH outcome through immune-mediated mechanisms. There was prominent reduced species diversity and microbiota overgrowth in the dysbiosis induced by ICH, which may reduce intestinal motility and increase gut permeability. In addition, recolonizing ICH mice with a normal health microbiota ameliorates functional deficits and neuroinflammation after ICH. Meanwhile, cell-tracking studies have demonstrated the migration of intestinal lymphocytes to the brain after ICH. In addition, therapeutic transplantation of fecal microbiota improves intestinal barrier damage. These results support the conclusion that the gut microbiome is a target of ICH-induced systemic alteration and is considered to have a substantial impact on ICH outcome. intracerebral hemorrhage neuroinflammation gut microbiota dysbiosis T cell Microbiology Guoyang Zhou verfasserin aut Bo Shao verfasserin aut Bo Shao verfasserin aut Hang Zhou verfasserin aut Chaoran Xu verfasserin aut Feng Yan verfasserin aut Lin Wang verfasserin aut Gao Chen verfasserin aut Jianru Li verfasserin aut Xiongjie Fu verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 12(2021) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:12 year:2021 https://doi.org/10.3389/fmicb.2021.647304 kostenfrei https://doaj.org/article/28b00b28516945f1b17a35222f4ec77c kostenfrei https://www.frontiersin.org/articles/10.3389/fmicb.2021.647304/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
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allfieldsSound	10.3389/fmicb.2021.647304 doi (DE-627)DOAJ053209427 (DE-599)DOAJ28b00b28516945f1b17a35222f4ec77c DE-627 ger DE-627 rakwb eng QR1-502 Xiaobo Yu verfasserin aut Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Intracerebral hemorrhage (ICH) induces a strong hematoma-related neuroinflammatory reaction and alters peripheral immune homeostasis. Recent research has found that gut microbiota plays a role in neurodegeneration and autoimmune diseases by regulating immune homeostasis and neuroinflammation. Therefore, we investigated the relationship between ICH, microbiota alteration, and immune responses after hematoma-induced acute brain injury. In our study, we used a mouse model of ICH, and 16S ribosomal RNA sequencing showed that ICH causes gut microbiota dysbiosis, which in turn affects ICH outcome through immune-mediated mechanisms. There was prominent reduced species diversity and microbiota overgrowth in the dysbiosis induced by ICH, which may reduce intestinal motility and increase gut permeability. In addition, recolonizing ICH mice with a normal health microbiota ameliorates functional deficits and neuroinflammation after ICH. Meanwhile, cell-tracking studies have demonstrated the migration of intestinal lymphocytes to the brain after ICH. In addition, therapeutic transplantation of fecal microbiota improves intestinal barrier damage. These results support the conclusion that the gut microbiome is a target of ICH-induced systemic alteration and is considered to have a substantial impact on ICH outcome. intracerebral hemorrhage neuroinflammation gut microbiota dysbiosis T cell Microbiology Guoyang Zhou verfasserin aut Bo Shao verfasserin aut Bo Shao verfasserin aut Hang Zhou verfasserin aut Chaoran Xu verfasserin aut Feng Yan verfasserin aut Lin Wang verfasserin aut Gao Chen verfasserin aut Jianru Li verfasserin aut Xiongjie Fu verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 12(2021) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:12 year:2021 https://doi.org/10.3389/fmicb.2021.647304 kostenfrei https://doaj.org/article/28b00b28516945f1b17a35222f4ec77c kostenfrei https://www.frontiersin.org/articles/10.3389/fmicb.2021.647304/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
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authorswithroles_txt_mv	Xiaobo Yu @@aut@@ Guoyang Zhou @@aut@@ Bo Shao @@aut@@ Hang Zhou @@aut@@ Chaoran Xu @@aut@@ Feng Yan @@aut@@ Lin Wang @@aut@@ Gao Chen @@aut@@ Jianru Li @@aut@@ Xiongjie Fu @@aut@@
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callnumber-first	Q - Science
author	Xiaobo Yu
spellingShingle	Xiaobo Yu misc QR1-502 misc intracerebral hemorrhage misc neuroinflammation misc gut microbiota misc dysbiosis misc T cell misc Microbiology Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice
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topic_title	QR1-502 Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice intracerebral hemorrhage neuroinflammation gut microbiota dysbiosis T cell
topic	misc QR1-502 misc intracerebral hemorrhage misc neuroinflammation misc gut microbiota misc dysbiosis misc T cell misc Microbiology
topic_unstemmed	misc QR1-502 misc intracerebral hemorrhage misc neuroinflammation misc gut microbiota misc dysbiosis misc T cell misc Microbiology
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title	Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice
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title_full	Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice
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author_browse	Xiaobo Yu Guoyang Zhou Bo Shao Hang Zhou Chaoran Xu Feng Yan Lin Wang Gao Chen Jianru Li Xiongjie Fu
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title_sort	gut microbiota dysbiosis induced by intracerebral hemorrhage aggravates neuroinflammation in mice
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title_auth	Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice
abstract	Intracerebral hemorrhage (ICH) induces a strong hematoma-related neuroinflammatory reaction and alters peripheral immune homeostasis. Recent research has found that gut microbiota plays a role in neurodegeneration and autoimmune diseases by regulating immune homeostasis and neuroinflammation. Therefore, we investigated the relationship between ICH, microbiota alteration, and immune responses after hematoma-induced acute brain injury. In our study, we used a mouse model of ICH, and 16S ribosomal RNA sequencing showed that ICH causes gut microbiota dysbiosis, which in turn affects ICH outcome through immune-mediated mechanisms. There was prominent reduced species diversity and microbiota overgrowth in the dysbiosis induced by ICH, which may reduce intestinal motility and increase gut permeability. In addition, recolonizing ICH mice with a normal health microbiota ameliorates functional deficits and neuroinflammation after ICH. Meanwhile, cell-tracking studies have demonstrated the migration of intestinal lymphocytes to the brain after ICH. In addition, therapeutic transplantation of fecal microbiota improves intestinal barrier damage. These results support the conclusion that the gut microbiome is a target of ICH-induced systemic alteration and is considered to have a substantial impact on ICH outcome.
abstractGer	Intracerebral hemorrhage (ICH) induces a strong hematoma-related neuroinflammatory reaction and alters peripheral immune homeostasis. Recent research has found that gut microbiota plays a role in neurodegeneration and autoimmune diseases by regulating immune homeostasis and neuroinflammation. Therefore, we investigated the relationship between ICH, microbiota alteration, and immune responses after hematoma-induced acute brain injury. In our study, we used a mouse model of ICH, and 16S ribosomal RNA sequencing showed that ICH causes gut microbiota dysbiosis, which in turn affects ICH outcome through immune-mediated mechanisms. There was prominent reduced species diversity and microbiota overgrowth in the dysbiosis induced by ICH, which may reduce intestinal motility and increase gut permeability. In addition, recolonizing ICH mice with a normal health microbiota ameliorates functional deficits and neuroinflammation after ICH. Meanwhile, cell-tracking studies have demonstrated the migration of intestinal lymphocytes to the brain after ICH. In addition, therapeutic transplantation of fecal microbiota improves intestinal barrier damage. These results support the conclusion that the gut microbiome is a target of ICH-induced systemic alteration and is considered to have a substantial impact on ICH outcome.
abstract_unstemmed	Intracerebral hemorrhage (ICH) induces a strong hematoma-related neuroinflammatory reaction and alters peripheral immune homeostasis. Recent research has found that gut microbiota plays a role in neurodegeneration and autoimmune diseases by regulating immune homeostasis and neuroinflammation. Therefore, we investigated the relationship between ICH, microbiota alteration, and immune responses after hematoma-induced acute brain injury. In our study, we used a mouse model of ICH, and 16S ribosomal RNA sequencing showed that ICH causes gut microbiota dysbiosis, which in turn affects ICH outcome through immune-mediated mechanisms. There was prominent reduced species diversity and microbiota overgrowth in the dysbiosis induced by ICH, which may reduce intestinal motility and increase gut permeability. In addition, recolonizing ICH mice with a normal health microbiota ameliorates functional deficits and neuroinflammation after ICH. Meanwhile, cell-tracking studies have demonstrated the migration of intestinal lymphocytes to the brain after ICH. In addition, therapeutic transplantation of fecal microbiota improves intestinal barrier damage. These results support the conclusion that the gut microbiome is a target of ICH-induced systemic alteration and is considered to have a substantial impact on ICH outcome.
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title_short	Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice
url	https://doi.org/10.3389/fmicb.2021.647304 https://doaj.org/article/28b00b28516945f1b17a35222f4ec77c https://www.frontiersin.org/articles/10.3389/fmicb.2021.647304/full https://doaj.org/toc/1664-302X
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Gut Microbiota Dysbiosis Induced by Intracerebral Hemorrhage Aggravates Neuroinflammation in Mice

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