Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation

Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct f...
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Autor*in:	Adrian J. Błażejewski [verfasserIn] Sophie Thiemann [verfasserIn] Alexander Schenk [verfasserIn] Marina C. Pils [verfasserIn] Eric J.C. Gálvez [verfasserIn] Urmi Roy [verfasserIn] Ulrike Heise [verfasserIn] Marcel R. de Zoete [verfasserIn] Richard A. Flavell [verfasserIn] Till Strowig [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis

Übergeordnetes Werk:	In: Cell Reports - Elsevier, 2015, 19(2017), 11, Seite 2319-2330
Übergeordnetes Werk:	volume:19 ; year:2017 ; number:11 ; pages:2319-2330

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.celrep.2017.05.058

Katalog-ID:	DOAJ041623762

Internformat


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520			\|a Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis.
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700	0		\|a Eric J.C. Gálvez \|e verfasserin \|4 aut
700	0		\|a Urmi Roy \|e verfasserin \|4 aut
700	0		\|a Ulrike Heise \|e verfasserin \|4 aut
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700	0		\|a Richard A. Flavell \|e verfasserin \|4 aut
700	0		\|a Till Strowig \|e verfasserin \|4 aut
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publishDate	2017
allfields	10.1016/j.celrep.2017.05.058 doi (DE-627)DOAJ041623762 (DE-599)DOAJ580ae42517974a368b8e6a328b0ee750 DE-627 ger DE-627 rakwb eng QH301-705.5 Adrian J. Błażejewski verfasserin aut Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis. caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis Biology (General) Sophie Thiemann verfasserin aut Alexander Schenk verfasserin aut Marina C. Pils verfasserin aut Eric J.C. Gálvez verfasserin aut Urmi Roy verfasserin aut Ulrike Heise verfasserin aut Marcel R. de Zoete verfasserin aut Richard A. Flavell verfasserin aut Till Strowig verfasserin aut In Cell Reports Elsevier, 2015 19(2017), 11, Seite 2319-2330 (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:19 year:2017 number:11 pages:2319-2330 https://doi.org/10.1016/j.celrep.2017.05.058 kostenfrei https://doaj.org/article/580ae42517974a368b8e6a328b0ee750 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124717307155 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 11 2319-2330
spelling	10.1016/j.celrep.2017.05.058 doi (DE-627)DOAJ041623762 (DE-599)DOAJ580ae42517974a368b8e6a328b0ee750 DE-627 ger DE-627 rakwb eng QH301-705.5 Adrian J. Błażejewski verfasserin aut Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis. caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis Biology (General) Sophie Thiemann verfasserin aut Alexander Schenk verfasserin aut Marina C. Pils verfasserin aut Eric J.C. Gálvez verfasserin aut Urmi Roy verfasserin aut Ulrike Heise verfasserin aut Marcel R. de Zoete verfasserin aut Richard A. Flavell verfasserin aut Till Strowig verfasserin aut In Cell Reports Elsevier, 2015 19(2017), 11, Seite 2319-2330 (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:19 year:2017 number:11 pages:2319-2330 https://doi.org/10.1016/j.celrep.2017.05.058 kostenfrei https://doaj.org/article/580ae42517974a368b8e6a328b0ee750 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124717307155 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 11 2319-2330
allfields_unstemmed	10.1016/j.celrep.2017.05.058 doi (DE-627)DOAJ041623762 (DE-599)DOAJ580ae42517974a368b8e6a328b0ee750 DE-627 ger DE-627 rakwb eng QH301-705.5 Adrian J. Błażejewski verfasserin aut Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis. caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis Biology (General) Sophie Thiemann verfasserin aut Alexander Schenk verfasserin aut Marina C. Pils verfasserin aut Eric J.C. Gálvez verfasserin aut Urmi Roy verfasserin aut Ulrike Heise verfasserin aut Marcel R. de Zoete verfasserin aut Richard A. Flavell verfasserin aut Till Strowig verfasserin aut In Cell Reports Elsevier, 2015 19(2017), 11, Seite 2319-2330 (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:19 year:2017 number:11 pages:2319-2330 https://doi.org/10.1016/j.celrep.2017.05.058 kostenfrei https://doaj.org/article/580ae42517974a368b8e6a328b0ee750 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124717307155 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 11 2319-2330
allfieldsGer	10.1016/j.celrep.2017.05.058 doi (DE-627)DOAJ041623762 (DE-599)DOAJ580ae42517974a368b8e6a328b0ee750 DE-627 ger DE-627 rakwb eng QH301-705.5 Adrian J. Błażejewski verfasserin aut Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis. caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis Biology (General) Sophie Thiemann verfasserin aut Alexander Schenk verfasserin aut Marina C. Pils verfasserin aut Eric J.C. Gálvez verfasserin aut Urmi Roy verfasserin aut Ulrike Heise verfasserin aut Marcel R. de Zoete verfasserin aut Richard A. Flavell verfasserin aut Till Strowig verfasserin aut In Cell Reports Elsevier, 2015 19(2017), 11, Seite 2319-2330 (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:19 year:2017 number:11 pages:2319-2330 https://doi.org/10.1016/j.celrep.2017.05.058 kostenfrei https://doaj.org/article/580ae42517974a368b8e6a328b0ee750 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124717307155 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 11 2319-2330
allfieldsSound	10.1016/j.celrep.2017.05.058 doi (DE-627)DOAJ041623762 (DE-599)DOAJ580ae42517974a368b8e6a328b0ee750 DE-627 ger DE-627 rakwb eng QH301-705.5 Adrian J. Błażejewski verfasserin aut Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis. caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis Biology (General) Sophie Thiemann verfasserin aut Alexander Schenk verfasserin aut Marina C. Pils verfasserin aut Eric J.C. Gálvez verfasserin aut Urmi Roy verfasserin aut Ulrike Heise verfasserin aut Marcel R. de Zoete verfasserin aut Richard A. Flavell verfasserin aut Till Strowig verfasserin aut In Cell Reports Elsevier, 2015 19(2017), 11, Seite 2319-2330 (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:19 year:2017 number:11 pages:2319-2330 https://doi.org/10.1016/j.celrep.2017.05.058 kostenfrei https://doaj.org/article/580ae42517974a368b8e6a328b0ee750 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124717307155 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 19 2017 11 2319-2330
language	English
source	In Cell Reports 19(2017), 11, Seite 2319-2330 volume:19 year:2017 number:11 pages:2319-2330
sourceStr	In Cell Reports 19(2017), 11, Seite 2319-2330 volume:19 year:2017 number:11 pages:2319-2330
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis Biology (General)
isfreeaccess_bool	true
container_title	Cell Reports
authorswithroles_txt_mv	Adrian J. Błażejewski @@aut@@ Sophie Thiemann @@aut@@ Alexander Schenk @@aut@@ Marina C. Pils @@aut@@ Eric J.C. Gálvez @@aut@@ Urmi Roy @@aut@@ Ulrike Heise @@aut@@ Marcel R. de Zoete @@aut@@ Richard A. Flavell @@aut@@ Till Strowig @@aut@@
publishDateDaySort_date	2017-01-01T00:00:00Z
hierarchy_top_id	684964562
id	DOAJ041623762
language_de	englisch
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callnumber-first	Q - Science
author	Adrian J. Błażejewski
spellingShingle	Adrian J. Błażejewski misc QH301-705.5 misc caspase-1 misc caspase-11 misc colitis misc inflammasome misc microbiota misc colon misc intestine misc DSS misc inflammation-induced tumorigenesis misc Biology (General) Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation
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topic_title	QH301-705.5 Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation caspase-1 caspase-11 colitis inflammasome microbiota colon intestine DSS inflammation-induced tumorigenesis
topic	misc QH301-705.5 misc caspase-1 misc caspase-11 misc colitis misc inflammasome misc microbiota misc colon misc intestine misc DSS misc inflammation-induced tumorigenesis misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc caspase-1 misc caspase-11 misc colitis misc inflammasome misc microbiota misc colon misc intestine misc DSS misc inflammation-induced tumorigenesis misc Biology (General)
topic_browse	misc QH301-705.5 misc caspase-1 misc caspase-11 misc colitis misc inflammasome misc microbiota misc colon misc intestine misc DSS misc inflammation-induced tumorigenesis misc Biology (General)
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title	Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation
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title_full	Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation
author_sort	Adrian J. Błażejewski
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author_browse	Adrian J. Błażejewski Sophie Thiemann Alexander Schenk Marina C. Pils Eric J.C. Gálvez Urmi Roy Ulrike Heise Marcel R. de Zoete Richard A. Flavell Till Strowig
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author-letter	Adrian J. Błażejewski
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title_sort	microbiota normalization reveals that canonical caspase-1 activation exacerbates chemically induced intestinal inflammation
callnumber	QH301-705.5
title_auth	Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation
abstract	Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis.
abstractGer	Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis.
abstract_unstemmed	Inflammasomes play a central role in regulating intestinal barrier function and immunity during steady state and disease. Because the discoveries of a passenger mutation and a colitogenic microbiota in the widely used caspase-1-deficient mouse strain have cast doubt on previously identified direct functions of caspase-1, we reassessed the role of caspase-1 in the intestine. To this end, we generated Casp1−/− and Casp11−/− mice and rederived them into an enhanced barrier facility to standardize the microbiota. We found that caspase-11 does not influence caspase-1-dependent processing of IL-18 in homeostasis and during DSS colitis. Deficiency of caspase-1, but not caspase-11, ameliorated the severity of DSS colitis independent of microbiota composition. Ablation of caspase-1 in intestinal epithelial cells was sufficient to protect mice against DSS colitis. Moreover, Casp1−/− mice developed fewer inflammation-induced intestinal tumors than control mice. These data show that canonical inflammasome activation controls caspase-1 activity, contributing to exacerbation of chemical-induced colitis.
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container_issue	11
title_short	Microbiota Normalization Reveals that Canonical Caspase-1 Activation Exacerbates Chemically Induced Intestinal Inflammation
url	https://doi.org/10.1016/j.celrep.2017.05.058 https://doaj.org/article/580ae42517974a368b8e6a328b0ee750 http://www.sciencedirect.com/science/article/pii/S2211124717307155 https://doaj.org/toc/2211-1247
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author2	Sophie Thiemann Alexander Schenk Marina C. Pils Eric J.C. Gálvez Urmi Roy Ulrike Heise Marcel R. de Zoete Richard A. Flavell Till Strowig
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up_date	2024-07-03T21:15:40.527Z
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