1918 pandemic influenza virus and Streptococcus pneumoniae co‐infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans
Identifieur interne : 000488 ( Istex/Curation ); précédent : 000487; suivant : 0004891918 pandemic influenza virus and Streptococcus pneumoniae co‐infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans
Auteurs : Kathie-Anne Walters [États-Unis] ; Felice D'Agnillo [États-Unis] ; Zong-Mei Sheng [États-Unis] ; Jason Kindrachuk [États-Unis] ; Louis M. Schwartzman [États-Unis] ; Rolf E. Kuestner [États-Unis] ; Daniel S. Chertow [États-Unis] ; Basil T. Golding [États-Unis] ; Jeffery K. Taubenberger [États-Unis] ; John C. Kash [États-Unis]Source :
- The Journal of Pathology [ 0022-3417 ] ; 2016-01.
Abstract
To study bacterial co‐infection following 1918 H1N1 influenza virus infection, mice were inoculated with the 1918 influenza virus, followed by Streptococcus pneumoniae (SP) 72 h later. Co‐infected mice exhibited markedly more severe disease, shortened survival time and more severe lung pathology, including widespread thrombi. Transcriptional profiling revealed activation of coagulation only in co‐infected mice, consistent with the extensive thrombogenesis observed. Immunohistochemistry showed extensive expression of tissue factor (F3) and prominent deposition of neutrophil elastase on endothelial and epithelial cells in co‐infected mice. Lung sections of SP‐positive 1918 autopsy cases showed extensive thrombi and prominent staining for F3 in alveolar macrophages, monocytes, neutrophils, endothelial and epithelial cells, in contrast to co‐infection‐positive 2009 pandemic H1N1 autopsy cases. This study reveals that a distinctive feature of 1918 influenza virus and SP co‐infection in mice and humans is extensive expression of tissue factor and activation of the extrinsic coagulation pathway leading to widespread pulmonary thrombosis. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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DOI: 10.1002/path.4638
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Schwartzman</name><affiliation wicri:level="1"><mods:affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda</wicri:regionArea></affiliation></author><author><name sortKey="Kuestner, Rolf E" sort="Kuestner, Rolf E" uniqKey="Kuestner R" first="Rolf E" last="Kuestner">Rolf E. Kuestner</name><affiliation wicri:level="1"><mods:affiliation>Institute for Systems Biology, WA, Seattle, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Institute for Systems Biology, WA, Seattle</wicri:regionArea></affiliation></author><author><name sortKey="Chertow, Daniel S" sort="Chertow, Daniel S" uniqKey="Chertow D" first="Daniel S" last="Chertow">Daniel S. Chertow</name><affiliation wicri:level="1"><mods:affiliation>Critical Care Medicine Department, National Institutes of Health (NIH), Bethesda, MD, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Critical Care Medicine Department, National Institutes of Health (NIH), Bethesda, MD</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda</wicri:regionArea></affiliation></author><author><name sortKey="Golding, Basil T" sort="Golding, Basil T" uniqKey="Golding B" first="Basil T" last="Golding">Basil T. Golding</name><affiliation wicri:level="1"><mods:affiliation>Laboratory of Biochemistry and Vascular Biology, Division of Hematology Research and Review, Center for Biologics Evaluation and Research, Office of Blood Research and Review, Food and Drug Administration, MD, Silver Spring, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Biochemistry and Vascular Biology, Division of Hematology Research and Review, Center for Biologics Evaluation and Research, Office of Blood Research and Review, Food and Drug Administration, MD, Silver Spring</wicri:regionArea></affiliation></author><author><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K" last="Taubenberger">Jeffery K. Taubenberger</name><affiliation wicri:level="1"><mods:affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda</wicri:regionArea></affiliation><affiliation><mods:affiliation>E-mail: taubenbergerj@niaid.nih.gov</mods:affiliation></affiliation></author><author><name sortKey="Kash, John C" sort="Kash, John C" uniqKey="Kash J" first="John C" last="Kash">John C. Kash</name><affiliation wicri:level="1"><mods:affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), MD, 20892, NIH, Bethesda</wicri:regionArea></affiliation><affiliation><mods:affiliation>E-mail: taubenbergerj@niaid.nih.gov</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The Journal of Pathology</title><title level="j" type="alt">THE JOURNAL OF PATHOLOGY</title><idno type="ISSN">0022-3417</idno><idno type="eISSN">1096-9896</idno><imprint><biblScope unit="vol">238</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="85">85</biblScope><biblScope unit="page" to="97">97</biblScope><biblScope unit="page-count">13</biblScope><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2016-01">2016-01</date></imprint><idno type="ISSN">0022-3417</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3417</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">To study bacterial co‐infection following 1918 H1N1 influenza virus infection, mice were inoculated with the 1918 influenza virus, followed by Streptococcus pneumoniae (SP) 72 h later. Co‐infected mice exhibited markedly more severe disease, shortened survival time and more severe lung pathology, including widespread thrombi. Transcriptional profiling revealed activation of coagulation only in co‐infected mice, consistent with the extensive thrombogenesis observed. Immunohistochemistry showed extensive expression of tissue factor (F3) and prominent deposition of neutrophil elastase on endothelial and epithelial cells in co‐infected mice. Lung sections of SP‐positive 1918 autopsy cases showed extensive thrombi and prominent staining for F3 in alveolar macrophages, monocytes, neutrophils, endothelial and epithelial cells, in contrast to co‐infection‐positive 2009 pandemic H1N1 autopsy cases. This study reveals that a distinctive feature of 1918 influenza virus and SP co‐infection in mice and humans is extensive expression of tissue factor and activation of the extrinsic coagulation pathway leading to widespread pulmonary thrombosis. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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