Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis

Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL...
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Autor*in:	Yang Liu [verfasserIn] Li-Hua Xing [verfasserIn] Fen-Xin Li [verfasserIn] Na Wang [verfasserIn] Yu-Ze Ma [verfasserIn] Jian-Wei Li [verfasserIn] Yu-Jing Wu [verfasserIn] Jing Liang [verfasserIn] Yu-Xin Lei [verfasserIn] Xue-Yin Wang [verfasserIn] Fan-Hua Meng [verfasserIn] Yong-Jun Yang [verfasserIn] Guang-Peng Li [verfasserIn] Xiao Wang [verfasserIn] Shui-Xing Yu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Molecular biology immune response microbiology bacteriology molecular microbiology

Übergeordnetes Werk:	In: iScience - Elsevier, 2019, 25(2022), 10, Seite 105121-
Übergeordnetes Werk:	volume:25 ; year:2022 ; number:10 ; pages:105121-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.isci.2022.105121

Katalog-ID:	DOAJ084910208

Internformat


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520			\|a Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis.
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author_variant	y l yl l h x lhx f x l fxl n w nw y z m yzm j w l jwl y j w yjw j l jl y x l yxl x y w xyw f h m fhm y j y yjy g p l gpl x w xw s x y sxy
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allfields	10.1016/j.isci.2022.105121 doi (DE-627)DOAJ084910208 (DE-599)DOAJ39fdf6b15edf46ec868549e35d62597f DE-627 ger DE-627 rakwb eng Yang Liu verfasserin aut Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis. Molecular biology immune response microbiology bacteriology molecular microbiology Science Q Li-Hua Xing verfasserin aut Fen-Xin Li verfasserin aut Na Wang verfasserin aut Yu-Ze Ma verfasserin aut Jian-Wei Li verfasserin aut Yu-Jing Wu verfasserin aut Jing Liang verfasserin aut Yu-Xin Lei verfasserin aut Xue-Yin Wang verfasserin aut Fan-Hua Meng verfasserin aut Yong-Jun Yang verfasserin aut Guang-Peng Li verfasserin aut Xiao Wang verfasserin aut Shui-Xing Yu verfasserin aut In iScience Elsevier, 2019 25(2022), 10, Seite 105121- (DE-627)1019532106 25890042 nnns volume:25 year:2022 number:10 pages:105121- https://doi.org/10.1016/j.isci.2022.105121 kostenfrei https://doaj.org/article/39fdf6b15edf46ec868549e35d62597f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004222013931 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2336 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2022 10 105121-
spelling	10.1016/j.isci.2022.105121 doi (DE-627)DOAJ084910208 (DE-599)DOAJ39fdf6b15edf46ec868549e35d62597f DE-627 ger DE-627 rakwb eng Yang Liu verfasserin aut Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis. Molecular biology immune response microbiology bacteriology molecular microbiology Science Q Li-Hua Xing verfasserin aut Fen-Xin Li verfasserin aut Na Wang verfasserin aut Yu-Ze Ma verfasserin aut Jian-Wei Li verfasserin aut Yu-Jing Wu verfasserin aut Jing Liang verfasserin aut Yu-Xin Lei verfasserin aut Xue-Yin Wang verfasserin aut Fan-Hua Meng verfasserin aut Yong-Jun Yang verfasserin aut Guang-Peng Li verfasserin aut Xiao Wang verfasserin aut Shui-Xing Yu verfasserin aut In iScience Elsevier, 2019 25(2022), 10, Seite 105121- (DE-627)1019532106 25890042 nnns volume:25 year:2022 number:10 pages:105121- https://doi.org/10.1016/j.isci.2022.105121 kostenfrei https://doaj.org/article/39fdf6b15edf46ec868549e35d62597f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004222013931 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2336 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2022 10 105121-
allfields_unstemmed	10.1016/j.isci.2022.105121 doi (DE-627)DOAJ084910208 (DE-599)DOAJ39fdf6b15edf46ec868549e35d62597f DE-627 ger DE-627 rakwb eng Yang Liu verfasserin aut Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis. Molecular biology immune response microbiology bacteriology molecular microbiology Science Q Li-Hua Xing verfasserin aut Fen-Xin Li verfasserin aut Na Wang verfasserin aut Yu-Ze Ma verfasserin aut Jian-Wei Li verfasserin aut Yu-Jing Wu verfasserin aut Jing Liang verfasserin aut Yu-Xin Lei verfasserin aut Xue-Yin Wang verfasserin aut Fan-Hua Meng verfasserin aut Yong-Jun Yang verfasserin aut Guang-Peng Li verfasserin aut Xiao Wang verfasserin aut Shui-Xing Yu verfasserin aut In iScience Elsevier, 2019 25(2022), 10, Seite 105121- (DE-627)1019532106 25890042 nnns volume:25 year:2022 number:10 pages:105121- https://doi.org/10.1016/j.isci.2022.105121 kostenfrei https://doaj.org/article/39fdf6b15edf46ec868549e35d62597f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004222013931 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2336 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2022 10 105121-
allfieldsGer	10.1016/j.isci.2022.105121 doi (DE-627)DOAJ084910208 (DE-599)DOAJ39fdf6b15edf46ec868549e35d62597f DE-627 ger DE-627 rakwb eng Yang Liu verfasserin aut Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis. Molecular biology immune response microbiology bacteriology molecular microbiology Science Q Li-Hua Xing verfasserin aut Fen-Xin Li verfasserin aut Na Wang verfasserin aut Yu-Ze Ma verfasserin aut Jian-Wei Li verfasserin aut Yu-Jing Wu verfasserin aut Jing Liang verfasserin aut Yu-Xin Lei verfasserin aut Xue-Yin Wang verfasserin aut Fan-Hua Meng verfasserin aut Yong-Jun Yang verfasserin aut Guang-Peng Li verfasserin aut Xiao Wang verfasserin aut Shui-Xing Yu verfasserin aut In iScience Elsevier, 2019 25(2022), 10, Seite 105121- (DE-627)1019532106 25890042 nnns volume:25 year:2022 number:10 pages:105121- https://doi.org/10.1016/j.isci.2022.105121 kostenfrei https://doaj.org/article/39fdf6b15edf46ec868549e35d62597f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004222013931 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2336 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2022 10 105121-
allfieldsSound	10.1016/j.isci.2022.105121 doi (DE-627)DOAJ084910208 (DE-599)DOAJ39fdf6b15edf46ec868549e35d62597f DE-627 ger DE-627 rakwb eng Yang Liu verfasserin aut Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis. Molecular biology immune response microbiology bacteriology molecular microbiology Science Q Li-Hua Xing verfasserin aut Fen-Xin Li verfasserin aut Na Wang verfasserin aut Yu-Ze Ma verfasserin aut Jian-Wei Li verfasserin aut Yu-Jing Wu verfasserin aut Jing Liang verfasserin aut Yu-Xin Lei verfasserin aut Xue-Yin Wang verfasserin aut Fan-Hua Meng verfasserin aut Yong-Jun Yang verfasserin aut Guang-Peng Li verfasserin aut Xiao Wang verfasserin aut Shui-Xing Yu verfasserin aut In iScience Elsevier, 2019 25(2022), 10, Seite 105121- (DE-627)1019532106 25890042 nnns volume:25 year:2022 number:10 pages:105121- https://doi.org/10.1016/j.isci.2022.105121 kostenfrei https://doaj.org/article/39fdf6b15edf46ec868549e35d62597f kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004222013931 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2336 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2022 10 105121-
language	English
source	In iScience 25(2022), 10, Seite 105121- volume:25 year:2022 number:10 pages:105121-
sourceStr	In iScience 25(2022), 10, Seite 105121- volume:25 year:2022 number:10 pages:105121-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Molecular biology immune response microbiology bacteriology molecular microbiology Science Q
isfreeaccess_bool	true
container_title	iScience
authorswithroles_txt_mv	Yang Liu @@aut@@ Li-Hua Xing @@aut@@ Fen-Xin Li @@aut@@ Na Wang @@aut@@ Yu-Ze Ma @@aut@@ Jian-Wei Li @@aut@@ Yu-Jing Wu @@aut@@ Jing Liang @@aut@@ Yu-Xin Lei @@aut@@ Xue-Yin Wang @@aut@@ Fan-Hua Meng @@aut@@ Yong-Jun Yang @@aut@@ Guang-Peng Li @@aut@@ Xiao Wang @@aut@@ Shui-Xing Yu @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	1019532106
id	DOAJ084910208
language_de	englisch
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author	Yang Liu
spellingShingle	Yang Liu misc Molecular biology misc immune response misc microbiology misc bacteriology misc molecular microbiology misc Science misc Q Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis
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topic_title	Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis Molecular biology immune response microbiology bacteriology molecular microbiology
topic	misc Molecular biology misc immune response misc microbiology misc bacteriology misc molecular microbiology misc Science misc Q
topic_unstemmed	misc Molecular biology misc immune response misc microbiology misc bacteriology misc molecular microbiology misc Science misc Q
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title	Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis
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title_full	Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis
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author_browse	Yang Liu Li-Hua Xing Fen-Xin Li Na Wang Yu-Ze Ma Jian-Wei Li Yu-Jing Wu Jing Liang Yu-Xin Lei Xue-Yin Wang Fan-Hua Meng Yong-Jun Yang Guang-Peng Li Xiao Wang Shui-Xing Yu
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title_sort	mixed lineage kinase-like protein protects against clostridium perfringens infection by enhancing nlrp3 inflammasome-extracellular traps axis
title_auth	Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis
abstract	Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis.
abstractGer	Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis.
abstract_unstemmed	Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. These findings highlight the requirement of MLKL for host defense against C. perfringens infection through enhancing NLRP3 inflammasome-extracellular traps axis.
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title_short	Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis
url	https://doi.org/10.1016/j.isci.2022.105121 https://doaj.org/article/39fdf6b15edf46ec868549e35d62597f http://www.sciencedirect.com/science/article/pii/S2589004222013931 https://doaj.org/toc/2589-0042
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author2Str	Li-Hua Xing Fen-Xin Li Na Wang Yu-Ze Ma Jian-Wei Li Yu-Jing Wu Jing Liang Yu-Xin Lei Xue-Yin Wang Fan-Hua Meng Yong-Jun Yang Guang-Peng Li Xiao Wang Shui-Xing Yu
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In C. perfringens gas gangrene and enterocolitis model, Mlkl−/− mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to C. perfringens infection. Mlkl deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases. Exogenous administration of recombinant IL-18 is able to rescue the susceptibility of Mlkl−/− mice. Notably, K+ efflux-dependent NLRP3 inflammasome signaling downstream of active MLKL promotes bacterial killing and clearance. Interestingly, the defect of bactericidal activity is also mediated by decreased classical extracellular trap formation in the absence of Mlkl. Our results demonstrate that MLKL mediates extracellular trap formation in a NLRP3 inflammasome-dependent manner. 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Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis

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