Long‐lived macrophage reprogramming drives spike protein‐mediated inflammasome activation in COVID‐19

Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike protein (S‐protein) primes inflammasome formation and release of mature interleukin‐1β (IL‐1β) in macrophages derived from COVID‐19 patients but not in...

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Published inEMBO molecular medicine Vol. 13; no. 8; pp. e14150 - n/a
Main Authors Theobald, Sebastian J, Simonis, Alexander, Georgomanolis, Theodoros, Kreer, Christoph, Zehner, Matthias, Eisfeld, Hannah S, Albert, Marie‐Christine, Chhen, Jason, Motameny, Susanne, Erger, Florian, Fischer, Julia, Malin, Jakob J, Gräb, Jessica, Winter, Sandra, Pouikli, Andromachi, David, Friederike, Böll, Boris, Koehler, Philipp, Vanshylla, Kanika, Gruell, Henning, Suárez, Isabelle, Hallek, Michael, Fätkenheuer, Gerd, Jung, Norma, Cornely, Oliver A, Lehmann, Clara, Tessarz, Peter, Altmüller, Janine, Nürnberg, Peter, Kashkar, Hamid, Klein, Florian, Koch, Manuel, Rybniker, Jan
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 09.08.2021
John Wiley & Sons, Inc
EMBO Press
John Wiley and Sons Inc
Springer Nature
Subjects
Adenosine triphosphate
Analysis
Antigens
Cell activation
Coronaviruses
COVID-19
COVID-19 vaccines
Cytokines
EMBO19
EMBO23
Epigenetic inheritance
Epigenetics
Gene expression
Health aspects
Immunogenicity
Immunological memory
Infections
inflammasome
Inflammasomes
Innate immunity
Kinases
macrophage
Macrophages
Medical research
Medicine, Experimental
Monocytes
NLRP3
Pathogens
Patients
Proteins
SARS‐CoV‐2
Severe acute respiratory syndrome coronavirus 2
Spike protein
Statistical analysis
Tumor necrosis factor-TNF
macrophage
NLRP3
innate immunity
SARS‐CoV‐2
inflammasome
Online AccessGet full text
ISSN1757-4676
1757-4684
1757-4684
DOI10.15252/emmm.202114150

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Abstract Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike protein (S‐protein) primes inflammasome formation and release of mature interleukin‐1β (IL‐1β) in macrophages derived from COVID‐19 patients but not in macrophages from healthy SARS‐CoV‐2 naïve individuals. Furthermore, longitudinal analyses reveal robust S‐protein‐driven inflammasome activation in macrophages isolated from convalescent COVID‐19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID‐19. Importantly, we show that S‐protein‐driven IL‐1β secretion from patient‐derived macrophages requires non‐specific monocyte pre‐activation in vivo to trigger NLRP3‐inflammasome signaling. Our findings reveal that SARS‐CoV‐2 infection causes profound and long‐lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS‐CoV‐2 S‐protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling. SYNOPSIS SARS‐CoV‐2 infection leads to hyperinflammatory syndromes in a subset of patients. We show that human primary macrophages require genome‐wide transcriptional modifications for pro‐inflammatory signaling upon stimulation with the SARS‐CoV‐2 surface glycoprotein (S‐protein). The SARS‐CoV‐2 spike protein drives NRLP3 inflammasome activation in COVID‐19 patient derived macrophages. Macrophages from SARS‐CoV‐2 naïve individuals fail to process and subsequently secrete IL‐1β upon stimulation with the S‐protein. The S‐protein is a pathogen‐associated molecular pattern (PAMP) requiring macrophage pre‐activation for NLRP3 inflammasome formation. Inflammasome activation and IL‐1β signaling represent attractive targets for pharmacological interventions in severe COVID‐19. Graphical Abstract SARS‐CoV‐2 infection leads to hyperinflammatory syndromes in a subset of patients. We show that human primary macrophages require genome‐wide transcriptional modifications for pro‐inflammatory signaling upon stimulation with the SARS‐CoV‐2 surface glycoprotein (S‐protein).
AbstractList Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1β (IL-1β) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naïve individuals. Furthermore, longitudinal analyses reveal robust S-protein-driven inflammasome activation in macrophages isolated from convalescent COVID-19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID-19. Importantly, we show that S-protein-driven IL-1β secretion from patient-derived macrophages requires non-specific monocyte pre-activation in vivo to trigger NLRP3-inflammasome signaling. Our findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling.
Abstract Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike protein (S‐protein) primes inflammasome formation and release of mature interleukin‐1β (IL‐1β) in macrophages derived from COVID‐19 patients but not in macrophages from healthy SARS‐CoV‐2 naïve individuals. Furthermore, longitudinal analyses reveal robust S‐protein‐driven inflammasome activation in macrophages isolated from convalescent COVID‐19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID‐19. Importantly, we show that S‐protein‐driven IL‐1β secretion from patient‐derived macrophages requires non‐specific monocyte pre‐activation in vivo to trigger NLRP3‐inflammasome signaling. Our findings reveal that SARS‐CoV‐2 infection causes profound and long‐lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS‐CoV‐2 S‐protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling.
Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike protein (S‐protein) primes inflammasome formation and release of mature interleukin‐1β (IL‐1β) in macrophages derived from COVID‐19 patients but not in macrophages from healthy SARS‐CoV‐2 naïve individuals. Furthermore, longitudinal analyses reveal robust S‐protein‐driven inflammasome activation in macrophages isolated from convalescent COVID‐19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID‐19. Importantly, we show that S‐protein‐driven IL‐1β secretion from patient‐derived macrophages requires non‐specific monocyte pre‐activation in vivo to trigger NLRP3‐inflammasome signaling. Our findings reveal that SARS‐CoV‐2 infection causes profound and long‐lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS‐CoV‐2 S‐protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling. SARS‐CoV‐2 infection leads to hyperinflammatory syndromes in a subset of patients. We show that human primary macrophages require genome‐wide transcriptional modifications for pro‐inflammatory signaling upon stimulation with the SARS‐CoV‐2 surface glycoprotein (S‐protein).
Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike protein (S‐protein) primes inflammasome formation and release of mature interleukin‐1β (IL‐1β) in macrophages derived from COVID‐19 patients but not in macrophages from healthy SARS‐CoV‐2 naïve individuals. Furthermore, longitudinal analyses reveal robust S‐protein‐driven inflammasome activation in macrophages isolated from convalescent COVID‐19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID‐19. Importantly, we show that S‐protein‐driven IL‐1β secretion from patient‐derived macrophages requires non‐specific monocyte pre‐activation in vivo to trigger NLRP3‐inflammasome signaling. Our findings reveal that SARS‐CoV‐2 infection causes profound and long‐lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS‐CoV‐2 S‐protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling. SYNOPSIS SARS‐CoV‐2 infection leads to hyperinflammatory syndromes in a subset of patients. We show that human primary macrophages require genome‐wide transcriptional modifications for pro‐inflammatory signaling upon stimulation with the SARS‐CoV‐2 surface glycoprotein (S‐protein). The SARS‐CoV‐2 spike protein drives NRLP3 inflammasome activation in COVID‐19 patient derived macrophages. Macrophages from SARS‐CoV‐2 naïve individuals fail to process and subsequently secrete IL‐1β upon stimulation with the S‐protein. The S‐protein is a pathogen‐associated molecular pattern (PAMP) requiring macrophage pre‐activation for NLRP3 inflammasome formation. Inflammasome activation and IL‐1β signaling represent attractive targets for pharmacological interventions in severe COVID‐19. SARS‐CoV‐2 infection leads to hyperinflammatory syndromes in a subset of patients. We show that human primary macrophages require genome‐wide transcriptional modifications for pro‐inflammatory signaling upon stimulation with the SARS‐CoV‐2 surface glycoprotein (S‐protein).
Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1β (IL-1β) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naïve individuals. Furthermore, longitudinal analyses reveal robust S-protein-driven inflammasome activation in macrophages isolated from convalescent COVID-19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID-19. Importantly, we show that S-protein-driven IL-1β secretion from patient-derived macrophages requires non-specific monocyte pre-activation in vivo to trigger NLRP3-inflammasome signaling. Our findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling.Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1β (IL-1β) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naïve individuals. Furthermore, longitudinal analyses reveal robust S-protein-driven inflammasome activation in macrophages isolated from convalescent COVID-19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID-19. Importantly, we show that S-protein-driven IL-1β secretion from patient-derived macrophages requires non-specific monocyte pre-activation in vivo to trigger NLRP3-inflammasome signaling. Our findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling.
Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike protein (S‐protein) primes inflammasome formation and release of mature interleukin‐1β (IL‐1β) in macrophages derived from COVID‐19 patients but not in macrophages from healthy SARS‐CoV‐2 naïve individuals. Furthermore, longitudinal analyses reveal robust S‐protein‐driven inflammasome activation in macrophages isolated from convalescent COVID‐19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID‐19. Importantly, we show that S‐protein‐driven IL‐1β secretion from patient‐derived macrophages requires non‐specific monocyte pre‐activation in vivo to trigger NLRP3‐inflammasome signaling. Our findings reveal that SARS‐CoV‐2 infection causes profound and long‐lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS‐CoV‐2 S‐protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling. SYNOPSIS SARS‐CoV‐2 infection leads to hyperinflammatory syndromes in a subset of patients. We show that human primary macrophages require genome‐wide transcriptional modifications for pro‐inflammatory signaling upon stimulation with the SARS‐CoV‐2 surface glycoprotein (S‐protein). The SARS‐CoV‐2 spike protein drives NRLP3 inflammasome activation in COVID‐19 patient derived macrophages. Macrophages from SARS‐CoV‐2 naïve individuals fail to process and subsequently secrete IL‐1β upon stimulation with the S‐protein. The S‐protein is a pathogen‐associated molecular pattern (PAMP) requiring macrophage pre‐activation for NLRP3 inflammasome formation. Inflammasome activation and IL‐1β signaling represent attractive targets for pharmacological interventions in severe COVID‐19. Graphical Abstract SARS‐CoV‐2 infection leads to hyperinflammatory syndromes in a subset of patients. We show that human primary macrophages require genome‐wide transcriptional modifications for pro‐inflammatory signaling upon stimulation with the SARS‐CoV‐2 surface glycoprotein (S‐protein).
Audience Academic
Author Koehler, Philipp
Winter, Sandra
Tessarz, Peter
Kashkar, Hamid
Böll, Boris
Vanshylla, Kanika
Zehner, Matthias
Albert, Marie‐Christine
Cornely, Oliver A
Altmüller, Janine
Chhen, Jason
Motameny, Susanne
Rybniker, Jan
David, Friederike
Gräb, Jessica
Georgomanolis, Theodoros
Pouikli, Andromachi
Klein, Florian
Simonis, Alexander
Nürnberg, Peter
Gruell, Henning
Hallek, Michael
Fätkenheuer, Gerd
Koch, Manuel
Erger, Florian
Fischer, Julia
Suárez, Isabelle
Lehmann, Clara
Jung, Norma
Kreer, Christoph
Eisfeld, Hannah S
Malin, Jakob J
Theobald, Sebastian J
AuthorAffiliation 4 Laboratory of Experimental Immunology Institute of Virology Faculty of Medicine and University Hospital of Cologne University of Cologne Cologne Germany
11 Medical Faculty Center for Biochemistry University of Cologne Cologne Germany
1 Department I of Internal Medicine Faculty of Medicine and University Hospital of Cologne University of Cologne Cologne Germany
10 Medical Faculty Institute for Dental Research and Oral Musculoskeletal Biology University of Cologne Cologne Germany
3 Faculty of Medicine and University Hospital of Cologne Cologne Center for Genomics (CCG) University of Cologne Cologne Germany
8 German Center for Infection Research (DZIF), Partner Site Bonn‐Cologne Cologne Germany
6 Institute for Medical Microbiology, Immunology and Hygiene (IMMIH) University of Cologne Cologne Germany
2 Faculty of Medicine and University Hospital of Cologne Center for Molecular Medicine Cologne (CMMC) University of Cologne Cologne Germany
5 Excellence Cluster on Cellular Stress Responses in Aging
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  orcidid: 0000-0001-8351-2690
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  fullname: Rybniker, Jan
  email: jan.rybniker@uk-koeln.de
  organization: Department I of Internal Medicine, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Faculty of Medicine and University Hospital of Cologne, Center for Molecular Medicine Cologne (CMMC), University of Cologne, German Center for Infection Research (DZIF), Partner Site Bonn‐Cologne
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Issue 8
Keywords macrophage
NLRP3
innate immunity
SARS‐CoV‐2
inflammasome
Language English
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Snippet Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike protein...
Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein...
Abstract Innate immunity triggers responsible for viral control or hyperinflammation in COVID‐19 are largely unknown. Here we show that the SARS‐CoV‐2 spike...
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pubmedcentral
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wiley
springer
SourceType Open Website
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StartPage e14150
SubjectTerms Adenosine triphosphate
Analysis
Antigens
Cell activation
Coronaviruses
COVID-19
COVID-19 vaccines
Cytokines
EMBO19
EMBO23
Epigenetic inheritance
Epigenetics
Gene expression
Health aspects
Immunogenicity
Immunological memory
Infections
inflammasome
Inflammasomes
Innate immunity
Kinases
macrophage
Macrophages
Medical research
Medicine, Experimental
Monocytes
NLRP3
Pathogens
Patients
Proteins
SARS‐CoV‐2
Severe acute respiratory syndrome coronavirus 2
Spike protein
Statistical analysis
Tumor necrosis factor-TNF
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Title Long‐lived macrophage reprogramming drives spike protein‐mediated inflammasome activation in COVID‐19
URI https://link.springer.com/article/10.15252/emmm.202114150
https://onlinelibrary.wiley.com/doi/abs/10.15252%2Femmm.202114150
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https://www.proquest.com/docview/2541789988
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Volume 13
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