Cited by 235Inflammasome and immune disordersCOVID-19 Clinical Research StudiesAutoimmune and Inflammatory Disorders Research

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SARS-CoV-2 infection and overactivation of Nlrp3 inflammasome as a trigger of cytokine “storm” and risk factor for damage of hematopoietic stem cells

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Ratajczak, Mariusz Z., Kucia, Magda·2020·Leukemia

DOI 10.1038/s41375-020-0887-9PMC PMC7262681

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Abstract

The scientific community faces an unexpected and urgent challenge related to the SARS-CoV-2 pandemic and is investigating the role of receptors involved in entry of this virus into cells as well as pathomechanisms leading to a cytokine “storm,” which in many cases ends in severe acute respiratory syndrome, fulminant myocarditis and kidney injury. An important question is if it may also damage hematopoietic stem progenitor cells?

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Fig. 1 The pathways of Nlrp3 inflammasome activation in response to SARS-CoV-2 infection that may lead to initiation of cytokine storm and pyroptosis in cells including HSPCs. a It is possible that, by binding to ACE2 via the spike protein, SARS-CoV-2 directly activates the Nlrp3 inflammasome. This possibility is currently being investigated by our team. b Activation of the renin–angiotensin–aldosterone system (RAAS) leads to elevated levels of angiotensin II, which, after binding to the AT1 receptor, activates the Nlrp3 inflammasome in target cells. c Finally, the N proteins of the SARS-CoV-2 virus may activate the ComC in an MBL–MASP-2-dependent manner, and the ComC cleavage fragments (the C3a and C5a anaphylatoxins), as well as the C5b/C9 membrane attack complex (MAC), may additionally activate the Nlrp3 inflammasome in cells. (Of note, MASP-2 also activates the coagulation cascade by converting prothrombin into thrombin). Overall, activation of all three of these pathways leads to activation of caspase 1, the release of the mature IL-1β and IL-18 cytokines, the insertion of gasdermin D channels in the cell membrane, and the release of danger-associated molecular pattern molecules (DAMPs), which amplify the innate immune response and may lead to cell death by pyroptosis.CC BY · PubMed Central

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2 retracted

Retraction Note to: SARS-CoV-2 infects T lymphocytes through its spike protein-mediated membrane fusion
Wang, X., Xu, W., Hu, G., Xia, S., Sun, Z., Liu, Z., Xie, Y., Zhang, R., Jiang, S., & Lu, L. (2020) · Cellular and Molecular Immunology · doi:10.1038/s41423-020-0498-4 · Cited by 175
Retracted
RETRACTED ARTICLE: SARS-CoV-2 infects T lymphocytes through its spike protein-mediated membrane fusion
Wang, X., Xu, W., Hu, G., Xia, S., Sun, Z., Liu, Z., Xie, Y., Zhang, R., Jiang, S., & Lu, L. (2020) · Cellular and Molecular Immunology · doi:10.1038/s41423-020-0424-9 · Cited by 162
Retracted
SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor
Hoffmann, M., Kleine-Weber, H., Schroeder, S., Krüger, N., Herrler, T., Erichsen, S., Schiergens, T. S., Herrler, G., Wu, N.-H., Nitsche, A., et al. (2020) · Cell · doi:10.1016/j.cell.2020.02.052 · Cited by 20,286 · cited 1×
“Moreover, as reported recently, S protein must be primed by transmembrane protease serine 2 (TMPRSS2) to facilitate interaction with ACE2 and the subsequent fusion of viral and cellular membranes [4].”
Background
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“lectin (MBL), which binds to SARS-CoV-2 proteins [12].”
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Renin-angiotensin-aldosterone system inhibitors in patients with Covid-19
Vaduganathan, M., Vardeny, O., Michel, T., McMurray, J. J. V., Pfeffer, M. A., & Solomon, S. D. (2020) · New England Journal of Medicine · doi:10.1056/nejmsr2005760 · Cited by 2,101
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“lung epithelial, kidney, and cardiac cells [1, 7].”
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Violi, F., Pastori, D., Cangemi, R., Pignatelli, P., & Loffredo, L. (2020) · Thrombosis and Haemostasis · doi:10.1055/s-0040-1710317 · Cited by 238 · cited 1×
“Importantly, activation of the ComC via the MBL–MASP-2 protease complex leads, in parallel, to activation of the coagulation cascade (CoaC), and in patients infected with SARS-CoV-2, activation of coagulation correlates with a worse prognosis [13].”
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Expression of angiotensin-converting enzyme (CD143) identifies and regulates primitive hemangioblasts derived from human pluripotent stem cells
Zambidis, E. T., Park, T. S., Yu, W., Tam, A. J., Levine, M. A., Yuan, X., Pryzhkova, M. V., & Péault, B. (2008) · Blood · doi:10.1182/blood-2008-03-144766 · Cited by 196 · cited 8×
“Moreover, since, as we already reported, HSPCs express Nlrp3 inflammasome components, it would be important to observe the long-term effects of SARS-CoV-2 infection on the hematopoietic stem cell compartment.”
BackgroundInfluential
The Nlrp3 inflammasome as a “rising star” in studies of normal and malignant hematopoiesis
Ratajczak, M. Z., Bujko, K., Cymer, M., Thapa, A., Adamiak, M., Ratajczak, J., Abdel-Latif, A. K., & Kucia, M. (2020) · Leukemia · doi:10.1038/s41375-020-0827-8 · Cited by 102 · cited 4×
“the Nlrp3 inflammasome in normal and malignant hematopoiesis [1].”
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Authors: Ratajczak, M. Z., & Kucia, M.
Affiliations: University of Louisville (US)
Corresponding author: Ratajczak, Mariusz Z.
ORCID: Ratajczak, Mariusz Z.
Kucia, Magda
Venue: Leukemia
Publisher: Springer Science and Business Media LLC
Published: 2020-06-01
Volume: 34
Issue: 7
Pages: 1726-1729
ISSN: 0887-6924 (ISSN-L)
1476-5551
DOI: 10.1038/s41375-020-0887-9
PMC: PMC7262681
OpenAlex: W3031438965
Semantic Scholar: 21891a793cf57a44dca049798218b329c5014a35
Cited by: 235
References: 16
Citations by year: 2026: 7 · 2025: 17 · 2024: 26 · 2023: 26 · 2022: 57 · 2021: 69 · 2020: 33
FWCI: 15.09
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0 (tdm)
creativecommons.org/licenses/by/4.0 (vor)
Locations: Leukemia (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (2R01 DK074720)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
Health Sciences › Medicine › Hematology › Autoimmune and Inflammatory Disorders Research
Keywords: SARS-CoV-2, NLRP3 inflammasome, cytokine storm, hematopoietic stem cells, COVID-19 pathogenesis, myocarditis, kidney injury, viral entry receptor
MeSH terms: Pyroptosis, NLR Family, Pyrin Domain-Containing 3 Protein, Betacoronavirus, Cytokine Release Syndrome, Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Furans, Gene Expression Regulation, Hematopoietic Stem Cells, Heterocyclic Compounds, 4 or More Rings, Humans, Immunity, Innate, Immunologic Factors, Indenes, Peptidyl-Dipeptidase A, Myocarditis, Pneumonia, Viral, Risk Factors, Sulfonamides, Sulfones, T-Lymphocytes, Cytokines, Coronavirus Infections, Severe Acute Respiratory Syndrome, Acute Kidney Injury, Inflammasomes, Pandemics, Spike Glycoprotein, Coronavirus

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SARS-CoV-2 infection and overactivation of Nlrp3 inflammasome as a trigger of cytokine “storm” and risk factor for damage of hematopoietic stem cells

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