β2 integrin mediates hantavirus-induced release of neutrophil extracellular traps

Rodent-borne hantaviruses are emerging human pathogens that cause severe human disease. The underlying mechanisms are not well understood, as hantaviruses replicate in endothelial and epithelial cells without causing any cytopathic effect. We demonstrate that hantaviruses strongly stimulated neutrop...

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Veröffentlicht in:	The Journal of experimental medicine Jg. 211; H. 7; S. 1485
Hauptverfasser:	Raftery, Martin J, Lalwani, Pritesh, Krautkrӓmer, Ellen, Peters, Thorsten, Scharffetter-Kochanek, Karin, Krüger, Renate, Hofmann, Jörg, Seeger, Karl, Krüger, Detlev H, Schönrich, Günther
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States 30.06.2014
Schlagworte:	Adenoviridae Animals Autoantibodies - genetics Autoantibodies - immunology CD18 Antigens - genetics CD18 Antigens - immunology CHO Cells Cricetinae Cricetulus Female Hantavirus - immunology Hantavirus Infections - genetics Hantavirus Infections - immunology Hantavirus Infections - pathology Humans Integrin alphaXbeta2 - genetics Integrin alphaXbeta2 - immunology Kidney Diseases - genetics Kidney Diseases - immunology Kidney Diseases - pathology Kidney Diseases - virology Lung Diseases - genetics Lung Diseases - immunology Lung Diseases - pathology Lung Diseases - virology Macrophage-1 Antigen - genetics Macrophage-1 Antigen - immunology Male Mice Mice, Mutant Strains Neutrophils - immunology Neutrophils - pathology
ISSN:	1540-9538, 1540-9538
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Abstract	Rodent-borne hantaviruses are emerging human pathogens that cause severe human disease. The underlying mechanisms are not well understood, as hantaviruses replicate in endothelial and epithelial cells without causing any cytopathic effect. We demonstrate that hantaviruses strongly stimulated neutrophils to release neutrophil extracellular traps (NETs). Hantavirus infection induced high systemic levels of circulating NETs in patients and this systemic NET overflow was accompanied by production of autoantibodies to nuclear antigens. Analysis of the responsible mechanism using neutrophils from β2 null mice identified β2 integrin receptors as a master switch for NET induction. Further experiments suggested that β2 integrin receptors such as complement receptor 3 (CR3) and 4 (CR4) may act as novel hantavirus entry receptors. Using adenoviruses, we confirmed that viral interaction with β2 integrin induced strong NET formation. Collectively, β2 integrin-mediated systemic NET overflow is a novel viral mechanism of immunopathology that may be responsible for characteristic aspects of hantavirus-associated disease such as kidney and lung damage.
AbstractList	Rodent-borne hantaviruses are emerging human pathogens that cause severe human disease. The underlying mechanisms are not well understood, as hantaviruses replicate in endothelial and epithelial cells without causing any cytopathic effect. We demonstrate that hantaviruses strongly stimulated neutrophils to release neutrophil extracellular traps (NETs). Hantavirus infection induced high systemic levels of circulating NETs in patients and this systemic NET overflow was accompanied by production of autoantibodies to nuclear antigens. Analysis of the responsible mechanism using neutrophils from β2 null mice identified β2 integrin receptors as a master switch for NET induction. Further experiments suggested that β2 integrin receptors such as complement receptor 3 (CR3) and 4 (CR4) may act as novel hantavirus entry receptors. Using adenoviruses, we confirmed that viral interaction with β2 integrin induced strong NET formation. Collectively, β2 integrin-mediated systemic NET overflow is a novel viral mechanism of immunopathology that may be responsible for characteristic aspects of hantavirus-associated disease such as kidney and lung damage.Rodent-borne hantaviruses are emerging human pathogens that cause severe human disease. The underlying mechanisms are not well understood, as hantaviruses replicate in endothelial and epithelial cells without causing any cytopathic effect. We demonstrate that hantaviruses strongly stimulated neutrophils to release neutrophil extracellular traps (NETs). Hantavirus infection induced high systemic levels of circulating NETs in patients and this systemic NET overflow was accompanied by production of autoantibodies to nuclear antigens. Analysis of the responsible mechanism using neutrophils from β2 null mice identified β2 integrin receptors as a master switch for NET induction. Further experiments suggested that β2 integrin receptors such as complement receptor 3 (CR3) and 4 (CR4) may act as novel hantavirus entry receptors. Using adenoviruses, we confirmed that viral interaction with β2 integrin induced strong NET formation. Collectively, β2 integrin-mediated systemic NET overflow is a novel viral mechanism of immunopathology that may be responsible for characteristic aspects of hantavirus-associated disease such as kidney and lung damage. Rodent-borne hantaviruses are emerging human pathogens that cause severe human disease. The underlying mechanisms are not well understood, as hantaviruses replicate in endothelial and epithelial cells without causing any cytopathic effect. We demonstrate that hantaviruses strongly stimulated neutrophils to release neutrophil extracellular traps (NETs). Hantavirus infection induced high systemic levels of circulating NETs in patients and this systemic NET overflow was accompanied by production of autoantibodies to nuclear antigens. Analysis of the responsible mechanism using neutrophils from β2 null mice identified β2 integrin receptors as a master switch for NET induction. Further experiments suggested that β2 integrin receptors such as complement receptor 3 (CR3) and 4 (CR4) may act as novel hantavirus entry receptors. Using adenoviruses, we confirmed that viral interaction with β2 integrin induced strong NET formation. Collectively, β2 integrin-mediated systemic NET overflow is a novel viral mechanism of immunopathology that may be responsible for characteristic aspects of hantavirus-associated disease such as kidney and lung damage.
Author	Peters, Thorsten Lalwani, Pritesh Hofmann, Jörg Schönrich, Günther Raftery, Martin J Scharffetter-Kochanek, Karin Krüger, Renate Krüger, Detlev H Seeger, Karl Krautkrӓmer, Ellen
Author_xml	– sequence: 1 givenname: Martin J surname: Raftery fullname: Raftery, Martin J organization: Institute of Medical Virology, Helmut-Ruska-Haus, Department of Pediatric Pneumology and Immunology, and Department of Pediatric Oncology and Hematology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany – sequence: 2 givenname: Pritesh surname: Lalwani fullname: Lalwani, Pritesh organization: Institute of Medical Virology, Helmut-Ruska-Haus, Department of Pediatric Pneumology and Immunology, and Department of Pediatric Oncology and Hematology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany – sequence: 3 givenname: Ellen surname: Krautkrӓmer fullname: Krautkrӓmer, Ellen organization: Department of Nephrology, University of Heidelberg, 69120 Heidelberg, Germany – sequence: 4 givenname: Thorsten surname: Peters fullname: Peters, Thorsten organization: Department of Dermatology and Allergic Diseases, University Hospital Ulm, 89081 Ulm, Germany – sequence: 5 givenname: Karin surname: Scharffetter-Kochanek fullname: Scharffetter-Kochanek, Karin organization: Department of Dermatology and Allergic Diseases, University Hospital Ulm, 89081 Ulm, Germany – sequence: 6 givenname: Renate surname: Krüger fullname: Krüger, Renate organization: Institute of Medical Virology, Helmut-Ruska-Haus, Department of Pediatric Pneumology and Immunology, and Department of Pediatric Oncology and Hematology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany – sequence: 7 givenname: Jörg surname: Hofmann fullname: Hofmann, Jörg organization: Institute of Medical Virology, Helmut-Ruska-Haus, Department of Pediatric Pneumology and Immunology, and Department of Pediatric Oncology and Hematology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany Division of Virology, Labor Berlin Charité-Vivantes GmbH, 13353 Berlin, Germany – sequence: 8 givenname: Karl surname: Seeger fullname: Seeger, Karl organization: Institute of Medical Virology, Helmut-Ruska-Haus, Department of Pediatric Pneumology and Immunology, and Department of Pediatric Oncology and Hematology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany – sequence: 9 givenname: Detlev H surname: Krüger fullname: Krüger, Detlev H organization: Institute of Medical Virology, Helmut-Ruska-Haus, Department of Pediatric Pneumology and Immunology, and Department of Pediatric Oncology and Hematology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany – sequence: 10 givenname: Günther surname: Schönrich fullname: Schönrich, Günther email: guenther.schoenrich@charite.de organization: Institute of Medical Virology, Helmut-Ruska-Haus, Department of Pediatric Pneumology and Immunology, and Department of Pediatric Oncology and Hematology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany guenther.schoenrich@charite.de
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/24889201$$D View this record in MEDLINE/PubMed
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Snippet	Rodent-borne hantaviruses are emerging human pathogens that cause severe human disease. The underlying mechanisms are not well understood, as hantaviruses...
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SubjectTerms	Adenoviridae Animals Autoantibodies - genetics Autoantibodies - immunology CD18 Antigens - genetics CD18 Antigens - immunology CHO Cells Cricetinae Cricetulus Female Hantavirus - immunology Hantavirus Infections - genetics Hantavirus Infections - immunology Hantavirus Infections - pathology Humans Integrin alphaXbeta2 - genetics Integrin alphaXbeta2 - immunology Kidney Diseases - genetics Kidney Diseases - immunology Kidney Diseases - pathology Kidney Diseases - virology Lung Diseases - genetics Lung Diseases - immunology Lung Diseases - pathology Lung Diseases - virology Macrophage-1 Antigen - genetics Macrophage-1 Antigen - immunology Male Mice Mice, Mutant Strains Neutrophils - immunology Neutrophils - pathology
Title	β2 integrin mediates hantavirus-induced release of neutrophil extracellular traps
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