Vascular occlusion by neutrophil extracellular traps in COVID-19
Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood. Samples were donated from hospitalized patients. Sera, plasma, and autopsy-deri...
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| Vydané v: | EBioMedicine Ročník 58; s. 102925 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Netherlands
Elsevier B.V
01.08.2020
Elsevier |
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| ISSN: | 2352-3964, 2352-3964 |
| On-line prístup: | Získať plný text |
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| Abstract | Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood.
Samples were donated from hospitalized patients. Sera, plasma, and autopsy-derived tissue sections were examined employing flow cytometry, enzyme-linked immunosorbent assays, and immunohistochemistry.
Here, we show that severe COVID-19 is characterized by a highly pronounced formation of neutrophil extracellular traps (NETs) inside the micro-vessels. Intravascular aggregation of NETs leads to rapid occlusion of the affected vessels, disturbed microcirculation, and organ damage. In severe COVID-19, neutrophil granulocytes are strongly activated and adopt a so-called low-density phenotype, prone to spontaneously form NETs. In accordance, markers indicating NET turnover are consistently increased in COVID-19 and linked to disease severity. Histopathology of the lungs and other organs from COVID-19 patients showed congestions of numerous micro-vessels by aggregated NETs associated with endothelial damage.
These data suggest that organ dysfunction in severe COVID-19 is associated with excessive NET formation and vascular damage.
Deutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-Stiftung |
|---|---|
| AbstractList | Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood.
Samples were donated from hospitalized patients. Sera, plasma, and autopsy-derived tissue sections were examined employing flow cytometry, enzyme-linked immunosorbent assays, and immunohistochemistry.
Here, we show that severe COVID-19 is characterized by a highly pronounced formation of neutrophil extracellular traps (NETs) inside the micro-vessels. Intravascular aggregation of NETs leads to rapid occlusion of the affected vessels, disturbed microcirculation, and organ damage. In severe COVID-19, neutrophil granulocytes are strongly activated and adopt a so-called low-density phenotype, prone to spontaneously form NETs. In accordance, markers indicating NET turnover are consistently increased in COVID-19 and linked to disease severity. Histopathology of the lungs and other organs from COVID-19 patients showed congestions of numerous micro-vessels by aggregated NETs associated with endothelial damage.
These data suggest that organ dysfunction in severe COVID-19 is associated with excessive NET formation and vascular damage.
Deutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-Stiftung. Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood. Samples were donated from hospitalized patients. Sera, plasma, and autopsy-derived tissue sections were examined employing flow cytometry, enzyme-linked immunosorbent assays, and immunohistochemistry. Here, we show that severe COVID-19 is characterized by a highly pronounced formation of neutrophil extracellular traps (NETs) inside the micro-vessels. Intravascular aggregation of NETs leads to rapid occlusion of the affected vessels, disturbed microcirculation, and organ damage. In severe COVID-19, neutrophil granulocytes are strongly activated and adopt a so-called low-density phenotype, prone to spontaneously form NETs. In accordance, markers indicating NET turnover are consistently increased in COVID-19 and linked to disease severity. Histopathology of the lungs and other organs from COVID-19 patients showed congestions of numerous micro-vessels by aggregated NETs associated with endothelial damage. These data suggest that organ dysfunction in severe COVID-19 is associated with excessive NET formation and vascular damage. Deutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-Stiftung AbstractBackgroundCoronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood. MethodsSamples were donated from hospitalized patients. Sera, plasma, and autopsy-derived tissue sections were examined employing flow cytometry, enzyme-linked immunosorbent assays, and immunohistochemistry. Patient findingsHere, we show that severe COVID-19 is characterized by a highly pronounced formation of neutrophil extracellular traps (NETs) inside the micro-vessels. Intravascular aggregation of NETs leads to rapid occlusion of the affected vessels, disturbed microcirculation, and organ damage. In severe COVID-19, neutrophil granulocytes are strongly activated and adopt a so-called low-density phenotype, prone to spontaneously form NETs. In accordance, markers indicating NET turnover are consistently increased in COVID-19 and linked to disease severity. Histopathology of the lungs and other organs from COVID-19 patients showed congestions of numerous micro-vessels by aggregated NETs associated with endothelial damage. InterpretationThese data suggest that organ dysfunction in severe COVID-19 is associated with excessive NET formation and vascular damage. FundingDeutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-Stiftung Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood.BACKGROUNDCoronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood.Samples were donated from hospitalized patients. Sera, plasma, and autopsy-derived tissue sections were examined employing flow cytometry, enzyme-linked immunosorbent assays, and immunohistochemistry.METHODSSamples were donated from hospitalized patients. Sera, plasma, and autopsy-derived tissue sections were examined employing flow cytometry, enzyme-linked immunosorbent assays, and immunohistochemistry.Here, we show that severe COVID-19 is characterized by a highly pronounced formation of neutrophil extracellular traps (NETs) inside the micro-vessels. Intravascular aggregation of NETs leads to rapid occlusion of the affected vessels, disturbed microcirculation, and organ damage. In severe COVID-19, neutrophil granulocytes are strongly activated and adopt a so-called low-density phenotype, prone to spontaneously form NETs. In accordance, markers indicating NET turnover are consistently increased in COVID-19 and linked to disease severity. Histopathology of the lungs and other organs from COVID-19 patients showed congestions of numerous micro-vessels by aggregated NETs associated with endothelial damage.PATIENT FINDINGSHere, we show that severe COVID-19 is characterized by a highly pronounced formation of neutrophil extracellular traps (NETs) inside the micro-vessels. Intravascular aggregation of NETs leads to rapid occlusion of the affected vessels, disturbed microcirculation, and organ damage. In severe COVID-19, neutrophil granulocytes are strongly activated and adopt a so-called low-density phenotype, prone to spontaneously form NETs. In accordance, markers indicating NET turnover are consistently increased in COVID-19 and linked to disease severity. Histopathology of the lungs and other organs from COVID-19 patients showed congestions of numerous micro-vessels by aggregated NETs associated with endothelial damage.These data suggest that organ dysfunction in severe COVID-19 is associated with excessive NET formation and vascular damage.INTERPRETATIONThese data suggest that organ dysfunction in severe COVID-19 is associated with excessive NET formation and vascular damage.Deutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-Stiftung.FUNDINGDeutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-Stiftung. Background: Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that trigger organ damage in COVID-19 are incompletely understood. Methods: Samples were donated from hospitalized patients. Sera, plasma, and autopsy-derived tissue sections were examined employing flow cytometry, enzyme-linked immunosorbent assays, and immunohistochemistry. Patient findings: Here, we show that severe COVID-19 is characterized by a highly pronounced formation of neutrophil extracellular traps (NETs) inside the micro-vessels. Intravascular aggregation of NETs leads to rapid occlusion of the affected vessels, disturbed microcirculation, and organ damage. In severe COVID-19, neutrophil granulocytes are strongly activated and adopt a so-called low-density phenotype, prone to spontaneously form NETs. In accordance, markers indicating NET turnover are consistently increased in COVID-19 and linked to disease severity. Histopathology of the lungs and other organs from COVID-19 patients showed congestions of numerous micro-vessels by aggregated NETs associated with endothelial damage. Interpretation: These data suggest that organ dysfunction in severe COVID-19 is associated with excessive NET formation and vascular damage. Funding: Deutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-Stiftung |
| ArticleNumber | 102925 |
| Author | Stürzl, Michael Hartmann, Arndt Herrmann, Martin Völkl, Simon Schett, Georg Evert, Katja Herrmann, Irmgard Lindemann, Aylin Kremer, Anita N. Muñoz, Luis E. Mahajan, Aparna Wehrfritz, Andreas Rieker, Ralf J. Naschberger, Elisabeth Singh, Jeeshan Knopf, Jasmin Neurath, Markus F. Staats, Léonie Amann, Kerstin Leppkes, Moritz Kremer, Andreas E. Schauer, Christine Falkeis, Christina |
| Author_xml | – sequence: 1 givenname: Moritz orcidid: 0000-0003-2311-090X surname: Leppkes fullname: Leppkes, Moritz email: moritz.leppkes@uk-erlangen.de organization: Department of Internal Medicine 1, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 2 givenname: Jasmin surname: Knopf fullname: Knopf, Jasmin organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 3 givenname: Elisabeth surname: Naschberger fullname: Naschberger, Elisabeth organization: Division of Molecular and Experimental Surgery, Translational Research Center, Department of Surgery, University Medical Center Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany – sequence: 4 givenname: Aylin surname: Lindemann fullname: Lindemann, Aylin organization: Department of Internal Medicine 1, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 5 givenname: Jeeshan surname: Singh fullname: Singh, Jeeshan organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 6 givenname: Irmgard surname: Herrmann fullname: Herrmann, Irmgard organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 7 givenname: Michael surname: Stürzl fullname: Stürzl, Michael organization: Division of Molecular and Experimental Surgery, Translational Research Center, Department of Surgery, University Medical Center Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany – sequence: 8 givenname: Léonie surname: Staats fullname: Staats, Léonie organization: Department of Internal Medicine 1, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 9 givenname: Aparna surname: Mahajan fullname: Mahajan, Aparna organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 10 givenname: Christine surname: Schauer fullname: Schauer, Christine organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 11 givenname: Anita N. surname: Kremer fullname: Kremer, Anita N. organization: Department of Internal Medicine 5, Hematology and Oncology, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 12 givenname: Simon surname: Völkl fullname: Völkl, Simon organization: Department of Internal Medicine 5, Hematology and Oncology, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 13 givenname: Kerstin surname: Amann fullname: Amann, Kerstin organization: Department of Nephropathology, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 14 givenname: Katja surname: Evert fullname: Evert, Katja organization: Institute of Pathology, University Medical Center Regensburg, Germany – sequence: 15 givenname: Christina surname: Falkeis fullname: Falkeis, Christina organization: Institut of Pathology, Klinikum Bayreuth, Germany – sequence: 16 givenname: Andreas surname: Wehrfritz fullname: Wehrfritz, Andreas organization: Department of Anaesthesiology, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 17 givenname: Ralf J. surname: Rieker fullname: Rieker, Ralf J. organization: Institute of Pathology, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 18 givenname: Arndt surname: Hartmann fullname: Hartmann, Arndt organization: Institute of Pathology, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 19 givenname: Andreas E. surname: Kremer fullname: Kremer, Andreas E. organization: Department of Internal Medicine 1, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 20 givenname: Markus F. surname: Neurath fullname: Neurath, Markus F. organization: Department of Internal Medicine 1, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 21 givenname: Luis E. surname: Muñoz fullname: Muñoz, Luis E. organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 22 givenname: Georg surname: Schett fullname: Schett, Georg organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany – sequence: 23 givenname: Martin surname: Herrmann fullname: Herrmann, Martin organization: Department of Internal Medicine 3, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32745993$$D View this record in MEDLINE/PubMed |
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| Snippet | Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The processes that... AbstractBackgroundCoronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs.... Background: Coronavirus induced disease 2019 (COVID-19) can be complicated by severe organ damage leading to dysfunction of the lungs and other organs. The... |
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| SubjectTerms | Advanced Basic Science Aggregated neutrophil extracellular traps Cells, Cultured Coagulopathy Coronavirus Infections - complications Coronavirus Infections - metabolism Coronavirus Infections - pathology COVID-19 Endothelialitis Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Extracellular Traps - metabolism Humans Immunothrombosis Internal Medicine Microvessels - metabolism Microvessels - pathology Neutrophils - metabolism Neutrophils - pathology Pandemics Pneumonia, Viral - complications Pneumonia, Viral - metabolism Pneumonia, Viral - pathology Research paper SARS-CoV-2 Thrombosis - etiology Thrombosis - metabolism Thrombosis - pathology |
| Title | Vascular occlusion by neutrophil extracellular traps in COVID-19 |
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