NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease

A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammator...
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Autor*in:	Rebecca Elena Mainz [verfasserIn] Stefanie Albers [verfasserIn] Madhuri Haque [verfasserIn] Roland Sonntag [verfasserIn] Nicole Simone Treichel [verfasserIn] Thomas Clavel [verfasserIn] Eicke Latz [verfasserIn] Kai Markus Schneider [verfasserIn] Christian Trautwein [verfasserIn] Tobias Otto [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	NLRP6 inflammasome alcoholic liver disease ALD gut microbiota intestinal microbiota

Übergeordnetes Werk:	In: Cells - MDPI AG, 2012, 11(2022), 2, p 182
Übergeordnetes Werk:	volume:11 ; year:2022 ; number:2, p 182

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/cells11020182

Katalog-ID:	DOAJ063272598

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520			\|a A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammatory mediators. The aim of this study was to evaluate a novel mouse model for ALD characterized by 8-week chronic-plus-binge ethanol administration and to investigate the role of NLRP6 inflammasome for intestinal homeostasis and ALD progression using <i<Nlrp6<sup<-/-</sup<</i< mice. We showed that chronic-plus-binge ethanol administration triggers hepatic steatosis, injury, and neutrophil infiltration. Furthermore, we discovered significant changes of intestinal microbial communities, including increased relative abundances of bacteria within the phyla <i<Bacteroidota</i< and <i<Campilobacterota</i<, as well as reduced <i<Firmicutes</i<. In this ALD model, inhibiting NLRP6 signaling had no effect on liver steatosis or damage, but had a minor impact on intestinal homeostasis via affecting intestinal epithelium function and gut microbiota. Surprisingly, <i<Nlrp6</i< loss resulted in significantly decreased hepatic immune cell infiltration. As a result, our novel mouse model encompasses several aspects of human ALD, such as intestinal dysbiosis. Interfering with NLRP6 inflammasome activity reduced hepatic immune cell recruitment, indicating a disease-aggravating role of NLRP6 during ALD.
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spelling	10.3390/cells11020182 doi (DE-627)DOAJ063272598 (DE-599)DOAJc36b46397fdd4fb39089d2520bf5296c DE-627 ger DE-627 rakwb eng QH573-671 Rebecca Elena Mainz verfasserin aut NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammatory mediators. The aim of this study was to evaluate a novel mouse model for ALD characterized by 8-week chronic-plus-binge ethanol administration and to investigate the role of NLRP6 inflammasome for intestinal homeostasis and ALD progression using <i<Nlrp6<sup<-/-</sup<</i< mice. We showed that chronic-plus-binge ethanol administration triggers hepatic steatosis, injury, and neutrophil infiltration. Furthermore, we discovered significant changes of intestinal microbial communities, including increased relative abundances of bacteria within the phyla <i<Bacteroidota</i< and <i<Campilobacterota</i<, as well as reduced <i<Firmicutes</i<. In this ALD model, inhibiting NLRP6 signaling had no effect on liver steatosis or damage, but had a minor impact on intestinal homeostasis via affecting intestinal epithelium function and gut microbiota. Surprisingly, <i<Nlrp6</i< loss resulted in significantly decreased hepatic immune cell infiltration. As a result, our novel mouse model encompasses several aspects of human ALD, such as intestinal dysbiosis. Interfering with NLRP6 inflammasome activity reduced hepatic immune cell recruitment, indicating a disease-aggravating role of NLRP6 during ALD. NLRP6 inflammasome alcoholic liver disease ALD gut microbiota intestinal microbiota Cytology Stefanie Albers verfasserin aut Madhuri Haque verfasserin aut Roland Sonntag verfasserin aut Nicole Simone Treichel verfasserin aut Thomas Clavel verfasserin aut Eicke Latz verfasserin aut Kai Markus Schneider verfasserin aut Christian Trautwein verfasserin aut Tobias Otto verfasserin aut In Cells MDPI AG, 2012 11(2022), 2, p 182 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:11 year:2022 number:2, p 182 https://doi.org/10.3390/cells11020182 kostenfrei https://doaj.org/article/c36b46397fdd4fb39089d2520bf5296c kostenfrei https://www.mdpi.com/2073-4409/11/2/182 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 11 2022 2, p 182
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allfieldsSound	10.3390/cells11020182 doi (DE-627)DOAJ063272598 (DE-599)DOAJc36b46397fdd4fb39089d2520bf5296c DE-627 ger DE-627 rakwb eng QH573-671 Rebecca Elena Mainz verfasserin aut NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammatory mediators. The aim of this study was to evaluate a novel mouse model for ALD characterized by 8-week chronic-plus-binge ethanol administration and to investigate the role of NLRP6 inflammasome for intestinal homeostasis and ALD progression using <i<Nlrp6<sup<-/-</sup<</i< mice. We showed that chronic-plus-binge ethanol administration triggers hepatic steatosis, injury, and neutrophil infiltration. Furthermore, we discovered significant changes of intestinal microbial communities, including increased relative abundances of bacteria within the phyla <i<Bacteroidota</i< and <i<Campilobacterota</i<, as well as reduced <i<Firmicutes</i<. In this ALD model, inhibiting NLRP6 signaling had no effect on liver steatosis or damage, but had a minor impact on intestinal homeostasis via affecting intestinal epithelium function and gut microbiota. Surprisingly, <i<Nlrp6</i< loss resulted in significantly decreased hepatic immune cell infiltration. As a result, our novel mouse model encompasses several aspects of human ALD, such as intestinal dysbiosis. Interfering with NLRP6 inflammasome activity reduced hepatic immune cell recruitment, indicating a disease-aggravating role of NLRP6 during ALD. NLRP6 inflammasome alcoholic liver disease ALD gut microbiota intestinal microbiota Cytology Stefanie Albers verfasserin aut Madhuri Haque verfasserin aut Roland Sonntag verfasserin aut Nicole Simone Treichel verfasserin aut Thomas Clavel verfasserin aut Eicke Latz verfasserin aut Kai Markus Schneider verfasserin aut Christian Trautwein verfasserin aut Tobias Otto verfasserin aut In Cells MDPI AG, 2012 11(2022), 2, p 182 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:11 year:2022 number:2, p 182 https://doi.org/10.3390/cells11020182 kostenfrei https://doaj.org/article/c36b46397fdd4fb39089d2520bf5296c kostenfrei https://www.mdpi.com/2073-4409/11/2/182 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 11 2022 2, p 182
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authorswithroles_txt_mv	Rebecca Elena Mainz @@aut@@ Stefanie Albers @@aut@@ Madhuri Haque @@aut@@ Roland Sonntag @@aut@@ Nicole Simone Treichel @@aut@@ Thomas Clavel @@aut@@ Eicke Latz @@aut@@ Kai Markus Schneider @@aut@@ Christian Trautwein @@aut@@ Tobias Otto @@aut@@
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callnumber-first	Q - Science
author	Rebecca Elena Mainz
spellingShingle	Rebecca Elena Mainz misc QH573-671 misc NLRP6 misc inflammasome misc alcoholic liver disease misc ALD misc gut microbiota misc intestinal microbiota misc Cytology NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease
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topic_title	QH573-671 NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease NLRP6 inflammasome alcoholic liver disease ALD gut microbiota intestinal microbiota
topic	misc QH573-671 misc NLRP6 misc inflammasome misc alcoholic liver disease misc ALD misc gut microbiota misc intestinal microbiota misc Cytology
topic_unstemmed	misc QH573-671 misc NLRP6 misc inflammasome misc alcoholic liver disease misc ALD misc gut microbiota misc intestinal microbiota misc Cytology
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title	NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease
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title_auth	NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease
abstract	A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammatory mediators. The aim of this study was to evaluate a novel mouse model for ALD characterized by 8-week chronic-plus-binge ethanol administration and to investigate the role of NLRP6 inflammasome for intestinal homeostasis and ALD progression using <i<Nlrp6<sup<-/-</sup<</i< mice. We showed that chronic-plus-binge ethanol administration triggers hepatic steatosis, injury, and neutrophil infiltration. Furthermore, we discovered significant changes of intestinal microbial communities, including increased relative abundances of bacteria within the phyla <i<Bacteroidota</i< and <i<Campilobacterota</i<, as well as reduced <i<Firmicutes</i<. In this ALD model, inhibiting NLRP6 signaling had no effect on liver steatosis or damage, but had a minor impact on intestinal homeostasis via affecting intestinal epithelium function and gut microbiota. Surprisingly, <i<Nlrp6</i< loss resulted in significantly decreased hepatic immune cell infiltration. As a result, our novel mouse model encompasses several aspects of human ALD, such as intestinal dysbiosis. Interfering with NLRP6 inflammasome activity reduced hepatic immune cell recruitment, indicating a disease-aggravating role of NLRP6 during ALD.
abstractGer	A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammatory mediators. The aim of this study was to evaluate a novel mouse model for ALD characterized by 8-week chronic-plus-binge ethanol administration and to investigate the role of NLRP6 inflammasome for intestinal homeostasis and ALD progression using <i<Nlrp6<sup<-/-</sup<</i< mice. We showed that chronic-plus-binge ethanol administration triggers hepatic steatosis, injury, and neutrophil infiltration. Furthermore, we discovered significant changes of intestinal microbial communities, including increased relative abundances of bacteria within the phyla <i<Bacteroidota</i< and <i<Campilobacterota</i<, as well as reduced <i<Firmicutes</i<. In this ALD model, inhibiting NLRP6 signaling had no effect on liver steatosis or damage, but had a minor impact on intestinal homeostasis via affecting intestinal epithelium function and gut microbiota. Surprisingly, <i<Nlrp6</i< loss resulted in significantly decreased hepatic immune cell infiltration. As a result, our novel mouse model encompasses several aspects of human ALD, such as intestinal dysbiosis. Interfering with NLRP6 inflammasome activity reduced hepatic immune cell recruitment, indicating a disease-aggravating role of NLRP6 during ALD.
abstract_unstemmed	A considerable percentage of the population is affected by alcoholic liver disease (ALD). It is characterized by inflammatory signals from the liver and other organs, such as the intestine. The NLR family pyrin domain containing 6 (NLRP6) inflammasome complex is one of the most important inflammatory mediators. The aim of this study was to evaluate a novel mouse model for ALD characterized by 8-week chronic-plus-binge ethanol administration and to investigate the role of NLRP6 inflammasome for intestinal homeostasis and ALD progression using <i<Nlrp6<sup<-/-</sup<</i< mice. We showed that chronic-plus-binge ethanol administration triggers hepatic steatosis, injury, and neutrophil infiltration. Furthermore, we discovered significant changes of intestinal microbial communities, including increased relative abundances of bacteria within the phyla <i<Bacteroidota</i< and <i<Campilobacterota</i<, as well as reduced <i<Firmicutes</i<. In this ALD model, inhibiting NLRP6 signaling had no effect on liver steatosis or damage, but had a minor impact on intestinal homeostasis via affecting intestinal epithelium function and gut microbiota. Surprisingly, <i<Nlrp6</i< loss resulted in significantly decreased hepatic immune cell infiltration. As a result, our novel mouse model encompasses several aspects of human ALD, such as intestinal dysbiosis. Interfering with NLRP6 inflammasome activity reduced hepatic immune cell recruitment, indicating a disease-aggravating role of NLRP6 during ALD.
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title_short	NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease
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NLRP6 Inflammasome Modulates Disease Progression in a Chronic-Plus-Binge Mouse Model of Alcoholic Liver Disease

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