Targeting neutrophils extracellular traps (NETs) reduces multiple organ injury in a COVID-19 mouse model

Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 p...

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Veröffentlicht in:	Respiratory research Jg. 24; H. 1; S. 66 - 11
Hauptverfasser:	Veras, Flavio P., Gomes, Giovanni F., Silva, Bruna M. S., Caetité, Diego B., Almeida, Cicero J. L. R., Silva, Camila Meirelles S., Schneider, Ayda H., Corneo, Emily S., Bonilha, Caio S., Batah, Sabrina S., Martins, Ronaldo, Arruda, Eurico, Fabro, Alexandre T., Alves-Filho, José C., Cunha, Thiago M., Cunha, Fernando Q.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	London BioMed Central 02.03.2023 BioMed Central Ltd Nature Publishing Group BMC
Schlagworte:	Acute Lung Injury Animal models Animals Antibodies Apoptosis Chemokines Clinical outcomes Cloning Coronaviruses COVID-19 COVID-19 Drug Treatment Cytokines Deoxyribonuclease Deoxyribonuclease I - pharmacology Deoxyribonuclease I - therapeutic use Disease Disease Models, Animal Extracellular Traps Health aspects Health services Heart diseases Histopathology Humans Infections Injuries Injury prevention Kidneys Kinases Laboratories Leukocytes (neutrophilic) Lung diseases Lungs Medicine Medicine & Public Health Mice Multiple organ failure Neutrophil extracellular traps Neutrophils Organ damage Pathophysiology Pneumology/Respiratory System Prevention Risk factors SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 Brazil COVID-19 SARS-CoV-2 Organ damage Neutrophil extracellular traps Neutrophils
ISSN:	1465-993X, 1465-9921, 1465-993X
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Abstract	Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. Methods Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers. Results DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro , which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I. Conclusions Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes.
AbstractList	Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. Methods Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers. Results DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro , which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I. Conclusions Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes. BackgroundCOVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. MethodsHere, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers.ResultsDNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I.ConclusionsTogether, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes. COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers. DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I. Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes. Abstract Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. Methods Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers. Results DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I. Conclusions Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes. COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment.BACKGROUNDCOVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment.Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers.METHODSHere, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers.DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I.RESULTSDNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I.Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes.CONCLUSIONSTogether, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes. Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. Methods Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers. Results DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I. Conclusions Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes. Keywords: Neutrophils, Neutrophil extracellular traps, Organ damage, COVID-19, SARS-CoV-2 COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps (NETs). COVID-19 treatment options are scarce. Previous work has shown an increase in NETs release in the lung and plasma of COVID-19 patients suggesting that drugs that prevent NETs formation or release could be potential therapeutic approaches for COVID-19 treatment. Here, we report the efficacy of NET-degrading DNase I treatment in a murine model of COVID-19. SARS-CoV-2-infected K18-hACE2 mice were performed for clinical sickness scores and lung pathology. Moreover, the levels of NETs were assessed and lung injuries were by histopathology and TUNEL assay. Finally, the injury in the heart and kidney was assessed by histopathology and biochemical-specific markers. DNase I decreased detectable levels of NETs, improved clinical disease, and reduced lung, heart, and kidney injuries in SARS-CoV-2-infected K18-hACE2 mice. Furthermore, our findings indicate a potentially deleterious role for NETs lung tissue in vivo and lung epithelial (A549) cells in vitro, which might explain part of the pathophysiology of severe COVID-19. This deleterious effect was diminished by the treatment with DNase I. Together, our results support the role of NETs in COVID-19 immunopathology and highlight NETs disruption pharmacological approaches as a potential strategy to ameliorate COVID-19 clinical outcomes.
ArticleNumber	66
Audience	Academic
Author	Silva, Camila Meirelles S. Cunha, Fernando Q. Bonilha, Caio S. Alves-Filho, José C. Gomes, Giovanni F. Martins, Ronaldo Cunha, Thiago M. Corneo, Emily S. Arruda, Eurico Batah, Sabrina S. Almeida, Cicero J. L. R. Caetité, Diego B. Schneider, Ayda H. Veras, Flavio P. Silva, Bruna M. S. Fabro, Alexandre T.
Author_xml	– sequence: 1 givenname: Flavio P. surname: Veras fullname: Veras, Flavio P. email: fprotasio@usp.br organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Department of BioMolecular Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, Universidade de São Paulo – sequence: 2 givenname: Giovanni F. surname: Gomes fullname: Gomes, Giovanni F. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 3 givenname: Bruna M. S. surname: Silva fullname: Silva, Bruna M. S. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 4 givenname: Diego B. surname: Caetité fullname: Caetité, Diego B. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 5 givenname: Cicero J. L. R. surname: Almeida fullname: Almeida, Cicero J. L. R. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 6 givenname: Camila Meirelles S. surname: Silva fullname: Silva, Camila Meirelles S. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 7 givenname: Ayda H. surname: Schneider fullname: Schneider, Ayda H. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 8 givenname: Emily S. surname: Corneo fullname: Corneo, Emily S. organization: Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina – sequence: 9 givenname: Caio S. surname: Bonilha fullname: Bonilha, Caio S. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 10 givenname: Sabrina S. surname: Batah fullname: Batah, Sabrina S. organization: Department of Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo – sequence: 11 givenname: Ronaldo surname: Martins fullname: Martins, Ronaldo organization: Virology Research Center, Ribeirão Preto Medical School, University of São Paulo – sequence: 12 givenname: Eurico surname: Arruda fullname: Arruda, Eurico organization: Virology Research Center, Ribeirão Preto Medical School, University of São Paulo – sequence: 13 givenname: Alexandre T. surname: Fabro fullname: Fabro, Alexandre T. organization: Department of Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo – sequence: 14 givenname: José C. surname: Alves-Filho fullname: Alves-Filho, José C. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 15 givenname: Thiago M. surname: Cunha fullname: Cunha, Thiago M. organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo – sequence: 16 givenname: Fernando Q. surname: Cunha fullname: Cunha, Fernando Q. email: fdqcunha@fmrp.usp.br organization: Center of Research in Inflammatory Diseases (CRID), Ribeirão Preto Medical School, University of São Paulo, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo
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Snippet	Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular... COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular traps... Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular... BackgroundCOVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil extracellular... Abstract Background COVID-19 is characterized by severe acute lung injury, which is associated with neutrophil infiltration and the release of neutrophil...
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SubjectTerms	Acute Lung Injury Animal models Animals Antibodies Apoptosis Chemokines Clinical outcomes Cloning Coronaviruses COVID-19 COVID-19 Drug Treatment Cytokines Deoxyribonuclease Deoxyribonuclease I - pharmacology Deoxyribonuclease I - therapeutic use Disease Disease Models, Animal Extracellular Traps Health aspects Health services Heart diseases Histopathology Humans Infections Injuries Injury prevention Kidneys Kinases Laboratories Leukocytes (neutrophilic) Lung diseases Lungs Medicine Medicine & Public Health Mice Multiple organ failure Neutrophil extracellular traps Neutrophils Organ damage Pathophysiology Pneumology/Respiratory System Prevention Risk factors SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2
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Title	Targeting neutrophils extracellular traps (NETs) reduces multiple organ injury in a COVID-19 mouse model
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