SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation
Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3...
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| Published in | Nature communications Vol. 12; no. 1; pp. 4664 - 17 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
02.08.2021
Nature Publishing Group Nature Portfolio |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1β and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses.
SARS-CoV-2 infection has been shown to drive NLRP3 inflammasome activation and thereby cytokine storm, but how it does so is unclear. Here the authors show that the viral N protein can bind to NLRP3, resulting in enhanced interaction with ASC and thereby with the NLRP3 inflammasome. |
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| AbstractList | Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1β and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses.SARS-CoV-2 infection has been shown to drive NLRP3 inflammasome activation and thereby cytokine storm, but how it does so is unclear. Here the authors show that the viral N protein can bind to NLRP3, resulting in enhanced interaction with ASC and thereby with the NLRP3 inflammasome. Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1β and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses. SARS-CoV-2 infection has been shown to drive NLRP3 inflammasome activation and thereby cytokine storm, but how it does so is unclear. Here the authors show that the viral N protein can bind to NLRP3, resulting in enhanced interaction with ASC and thereby with the NLRP3 inflammasome. Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1β and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses.Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1β and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses. Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1β and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses. SARS-CoV-2 infection has been shown to drive NLRP3 inflammasome activation and thereby cytokine storm, but how it does so is unclear. Here the authors show that the viral N protein can bind to NLRP3, resulting in enhanced interaction with ASC and thereby with the NLRP3 inflammasome. |
| ArticleNumber | 4664 |
| Author | Luo, Zhen Xiao, Feng Zhang, Qiwei Pan, Pan Li, Geng Wang, Jun Wan, Pin Lei, Zhiwei Shen, Miaomiao Yu, Zhenyang Wang, Zhenwei Zhang, Jing Chen, Xin Tian, Mingfu Chen, Weijie Wu, Jianguo Jia, Yaling Wang, Wenbiao Chen, Keli Ge, Weiwei Xu, Meng Li, Yongkui |
| Author_xml | – sequence: 1 givenname: Pan orcidid: 0000-0002-7214-1393 surname: Pan fullname: Pan, Pan organization: The First Affiliated Hospital of Jinan University, Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 2 givenname: Miaomiao orcidid: 0000-0002-9680-1130 surname: Shen fullname: Shen, Miaomiao organization: State Key Laboratory of Virology, College of Life Sciences, Wuhan University – sequence: 3 givenname: Zhenyang orcidid: 0000-0003-1776-9230 surname: Yu fullname: Yu, Zhenyang organization: State Key Laboratory of Virology, College of Life Sciences, Wuhan University – sequence: 4 givenname: Weiwei orcidid: 0000-0002-8397-7903 surname: Ge fullname: Ge, Weiwei organization: State Key Laboratory of Virology, College of Life Sciences, Wuhan University – sequence: 5 givenname: Keli orcidid: 0000-0002-0125-3646 surname: Chen fullname: Chen, Keli organization: State Key Laboratory of Virology, College of Life Sciences, Wuhan University – sequence: 6 givenname: Mingfu orcidid: 0000-0003-0122-6397 surname: Tian fullname: Tian, Mingfu organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, State Key Laboratory of Virology, College of Life Sciences, Wuhan University – sequence: 7 givenname: Feng orcidid: 0000-0002-7895-7940 surname: Xiao fullname: Xiao, Feng organization: State Key Laboratory of Virology, College of Life Sciences, Wuhan University – sequence: 8 givenname: Zhenwei orcidid: 0000-0002-1627-6082 surname: Wang fullname: Wang, Zhenwei organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 9 givenname: Jun orcidid: 0000-0003-2554-7216 surname: Wang fullname: Wang, Jun organization: The Affiliated ShunDe Hospital of Jinan University – sequence: 10 givenname: Yaling orcidid: 0000-0003-0025-7271 surname: Jia fullname: Jia, Yaling organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 11 givenname: Wenbiao orcidid: 0000-0003-4944-764X surname: Wang fullname: Wang, Wenbiao organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 12 givenname: Pin orcidid: 0000-0001-5374-2356 surname: Wan fullname: Wan, Pin organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 13 givenname: Jing orcidid: 0000-0003-1380-3948 surname: Zhang fullname: Zhang, Jing organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 14 givenname: Weijie orcidid: 0000-0002-4559-6317 surname: Chen fullname: Chen, Weijie organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 15 givenname: Zhiwei orcidid: 0000-0002-9406-2127 surname: Lei fullname: Lei, Zhiwei organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 16 givenname: Xin surname: Chen fullname: Chen, Xin organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University – sequence: 17 givenname: Zhen orcidid: 0000-0002-1142-2845 surname: Luo fullname: Luo, Zhen organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Foshan Institute of Medical Microbiology – sequence: 18 givenname: Qiwei orcidid: 0000-0002-2770-111X surname: Zhang fullname: Zhang, Qiwei organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Foshan Institute of Medical Microbiology – sequence: 19 givenname: Meng orcidid: 0000-0001-7387-0734 surname: Xu fullname: Xu, Meng organization: The First Affiliated Hospital of Jinan University – sequence: 20 givenname: Geng orcidid: 0000-0002-2441-2427 surname: Li fullname: Li, Geng email: lg@gzucm.edu.cn organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Foshan Institute of Medical Microbiology – sequence: 21 givenname: Yongkui orcidid: 0000-0002-1532-4855 surname: Li fullname: Li, Yongkui email: lyk070@jnu.edu.cn organization: Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Foshan Institute of Medical Microbiology – sequence: 22 givenname: Jianguo orcidid: 0000-0002-8326-2895 surname: Wu fullname: Wu, Jianguo email: jwu898@jnu.edu.cn organization: The First Affiliated Hospital of Jinan University, Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Foshan Institute of Medical Microbiology |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34341353$$D View this record in MEDLINE/PubMed |
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| Snippet | Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to... SARS-CoV-2 infection has been shown to drive NLRP3 inflammasome activation and thereby cytokine storm, but how it does so is unclear. Here the authors show... |
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| SubjectTerms | 13/109 13/21 13/51 13/89 14/19 38 42 45 45/111 631/250/254 631/250/256/2177 631/326/596/2553 82/51 96/95 Animal models Animals Caspase-1 Cells, Cultured Coronavirus Nucleocapsid Proteins - metabolism Coronaviruses COVID-19 COVID-19 - metabolism COVID-19 - virology Cytokine storm Cytokines Cytokines - metabolism HEK293 Cells Humanities and Social Sciences Humans IL-1β Infections Inflammasomes Inflammasomes - genetics Inflammasomes - metabolism Inflammation Inflammation - metabolism Inhibitors Interleukin 6 Lung Injury - genetics Lung Injury - metabolism Lungs Male Mice Mice, Inbred C57BL Mice, Knockout multidisciplinary N protein NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Phosphoproteins - metabolism Protein Binding Proteins SARS-CoV-2 - metabolism SARS-CoV-2 - physiology Science Science (multidisciplinary) Sepsis Severe acute respiratory syndrome coronavirus 2 THP-1 Cells Viral diseases |
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| Title | SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation |
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