Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19

Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV...

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Vydáno v:	Nature reviews. Immunology Ročník 21; číslo 5; s. 319 - 329
Hlavní autoři:	Bonaventura, Aldo, Vecchié, Alessandra, Dagna, Lorenzo, Martinod, Kimberly, Dixon, Dave L., Van Tassell, Benjamin W., Dentali, Francesco, Montecucco, Fabrizio, Massberg, Steffen, Levi, Marcel, Abbate, Antonio
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 01.05.2021 Nature Publishing Group
Témata:	631/250/127 631/250/2499 631/250/2500 631/250/255/2514 631/250/262 Biomedical and Life Sciences Biomedicine Blood clot Blood Coagulation - immunology Blood Platelets - immunology Coronaviruses COVID-19 COVID-19 - immunology COVID-19 - pathology Critical Illness - therapy Cytokine Release Syndrome - immunology Cytokine Release Syndrome - pathology Development and progression Drug development Endothelium Endothelium, Vascular - pathology Fibrinolytic Agents - therapeutic use Health aspects Humans Immune response Immune system Immunity, Innate - immunology Immunology Immunosuppressive agents Infections Leukocytes (neutrophilic) Lung - blood supply Lung - pathology Lung - virology Monocytes Monocytes - immunology Neutrophils - immunology Patients Perspective Respiratory distress syndrome SARS-CoV-2 - immunology SARS-CoV-2 - pathogenicity Severe acute respiratory syndrome coronavirus 2 Thrombosis Venous Thrombosis - immunology Venous Thrombosis - pathology Venous Thrombosis - prevention & control United States
ISSN:	1474-1733, 1474-1741, 1474-1741
On-line přístup:	Získat plný text
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Abstract	Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease. Here, the authors propose that SARS-CoV-2 induces a prothrombotic state, with dysregulated immunothrombosis in lung microvessels and endothelial injury, which drive the clinical manifestations of severe COVID-19. They discuss potential antithrombotic and immunomodulating drugs that are being considered in the treatment of patients with COVID-19.
AbstractList	Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease. Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease.Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease. Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease.Here, the authors propose that SARS-CoV-2 induces a prothrombotic state, with dysregulated immunothrombosis in lung microvessels and endothelial injury, which drive the clinical manifestations of severe COVID-19. They discuss potential antithrombotic and immunomodulating drugs that are being considered in the treatment of patients with COVID-19. Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease. Here, the authors propose that SARS-CoV-2 induces a prothrombotic state, with dysregulated immunothrombosis in lung microvessels and endothelial injury, which drive the clinical manifestations of severe COVID-19. They discuss potential antithrombotic and immunomodulating drugs that are being considered in the treatment of patients with COVID-19.
Audience	Academic
Author	Van Tassell, Benjamin W. Dentali, Francesco Levi, Marcel Montecucco, Fabrizio Vecchié, Alessandra Dixon, Dave L. Martinod, Kimberly Bonaventura, Aldo Massberg, Steffen Abbate, Antonio Dagna, Lorenzo
Author_xml	– sequence: 1 givenname: Aldo orcidid: 0000-0002-4747-5535 surname: Bonaventura fullname: Bonaventura, Aldo email: aldo.bonaventura@asst-settelaghi.it organization: Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Department of Internal Medicine, ASST dei Sette Laghi – sequence: 2 givenname: Alessandra surname: Vecchié fullname: Vecchié, Alessandra organization: Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Department of Internal Medicine, ASST dei Sette Laghi – sequence: 3 givenname: Lorenzo surname: Dagna fullname: Dagna, Lorenzo organization: Unit of Immunology, Rheumatology, Allergy and Rare Diseases, IRCCS San Raffaele Scientific Institute, Vita-Salute San Raffaele University – sequence: 4 givenname: Kimberly orcidid: 0000-0002-1026-6107 surname: Martinod fullname: Martinod, Kimberly organization: Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences, KU Leuven – sequence: 5 givenname: Dave L. surname: Dixon fullname: Dixon, Dave L. organization: Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Department of Pharmacotherapy and Outcome Science, School of Pharmacy, Virginia Commonwealth University – sequence: 6 givenname: Benjamin W. surname: Van Tassell fullname: Van Tassell, Benjamin W. organization: Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Department of Pharmacotherapy and Outcome Science, School of Pharmacy, Virginia Commonwealth University – sequence: 7 givenname: Francesco surname: Dentali fullname: Dentali, Francesco organization: Department of Medicine and Surgery, Insubria University – sequence: 8 givenname: Fabrizio orcidid: 0000-0003-0823-8729 surname: Montecucco fullname: Montecucco, Fabrizio organization: IRCCS Ospedale Policlinico San Martino Genova — Italian Cardiovascular Network, First Clinic of Internal Medicine, Department of Internal Medicine and Centre of Excellence for Biomedical Research (CEBR), University of Genoa – sequence: 9 givenname: Steffen orcidid: 0000-0001-7387-3986 surname: Massberg fullname: Massberg, Steffen organization: Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V., Partner Site Munich Heart Alliance, Medizinische Klinik und Poliklinik I, Klinikum der Universität, Ludwig-Maximilians-Universität – sequence: 10 givenname: Marcel surname: Levi fullname: Levi, Marcel organization: Department of Medicine and Cardio-metabolic Programme — NIHR UCLH/UCL BRC, University College London Hospitals NHS Foundation Trust – sequence: 11 givenname: Antonio surname: Abbate fullname: Abbate, Antonio organization: Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University
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Snippet	Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with...
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SubjectTerms	631/250/127 631/250/2499 631/250/2500 631/250/255/2514 631/250/262 Biomedical and Life Sciences Biomedicine Blood clot Blood Coagulation - immunology Blood Platelets - immunology Coronaviruses COVID-19 COVID-19 - immunology COVID-19 - pathology Critical Illness - therapy Cytokine Release Syndrome - immunology Cytokine Release Syndrome - pathology Development and progression Drug development Endothelium Endothelium, Vascular - pathology Fibrinolytic Agents - therapeutic use Health aspects Humans Immune response Immune system Immunity, Innate - immunology Immunology Immunosuppressive agents Infections Leukocytes (neutrophilic) Lung - blood supply Lung - pathology Lung - virology Monocytes Monocytes - immunology Neutrophils - immunology Patients Perspective Respiratory distress syndrome SARS-CoV-2 - immunology SARS-CoV-2 - pathogenicity Severe acute respiratory syndrome coronavirus 2 Thrombosis Venous Thrombosis - immunology Venous Thrombosis - pathology Venous Thrombosis - prevention & control
Title	Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19
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