1918 pandemic influenza virus and Streptococcus pneumoniae co-infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans.
Identifieur interne : 001A85 ( Ncbi/Merge ); précédent : 001A84; suivant : 001A861918 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 [ 1096-9896 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Co-infection (), Coagulation sanguine, Embolie pulmonaire (anatomopathologie), Embolie pulmonaire (microbiologie), Femelle, Grippe humaine (), Grippe humaine (anatomopathologie), Grippe humaine (microbiologie), Humains, Immunohistochimie, Infections à Orthomyxoviridae (), Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (microbiologie), Infections à pneumocoques (), Infections à pneumocoques (anatomopathologie), Infections à pneumocoques (microbiologie), Modèles animaux de maladie humaine, Pandémie de grippe de 1918-1919, RT-PCR, Souris, Souris de lignée BALB C, Sous-type H1N1 du virus de la grippe A, Streptococcus pneumoniae, Séquençage par oligonucléotides en batterie.
- MESH :
- anatomopathologie : Embolie pulmonaire, Grippe humaine, Infections à Orthomyxoviridae, Infections à pneumocoques.
- microbiologie : Embolie pulmonaire, Grippe humaine, Infections à Orthomyxoviridae, Infections à pneumocoques.
- Animaux, Co-infection, Coagulation sanguine, Femelle, Grippe humaine, Humains, Immunohistochimie, Infections à Orthomyxoviridae, Infections à pneumocoques, Modèles animaux de maladie humaine, Pandémie de grippe de 1918-1919, RT-PCR, Souris, Souris de lignée BALB C, Sous-type H1N1 du virus de la grippe A, Streptococcus pneumoniae, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Animals, Blood Coagulation, Coinfection (complications), Disease Models, Animal, Female, Humans, Immunohistochemistry, Influenza A Virus, H1N1 Subtype, Influenza Pandemic, 1918-1919, Influenza, Human (complications), Influenza, Human (microbiology), Influenza, Human (pathology), Mice, Mice, Inbred BALB C, Oligonucleotide Array Sequence Analysis, Orthomyxoviridae Infections (complications), Orthomyxoviridae Infections (microbiology), Orthomyxoviridae Infections (pathology), Pneumococcal Infections (complications), Pneumococcal Infections (microbiology), Pneumococcal Infections (pathology), Pulmonary Embolism (microbiology), Pulmonary Embolism (pathology), Reverse Transcriptase Polymerase Chain Reaction, Streptococcus pneumoniae.
- MESH :
- complications : Coinfection, Influenza, Human, Orthomyxoviridae Infections, Pneumococcal Infections.
- microbiology : Influenza, Human, Orthomyxoviridae Infections, Pneumococcal Infections, Pulmonary Embolism.
- pathology : Influenza, Human, Orthomyxoviridae Infections, Pneumococcal Infections, Pulmonary Embolism.
- Animals, Blood Coagulation, Disease Models, Animal, Female, Humans, Immunohistochemistry, Influenza A Virus, H1N1 Subtype, Influenza Pandemic, 1918-1919, Mice, Mice, Inbred BALB C, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, Streptococcus pneumoniae.
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.
DOI: 10.1002/path.4638
PubMed: 26383585
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pubmed:26383585Le document en format XML
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<term>Blood Coagulation</term>
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<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Immunohistochemistry</term>
<term>Influenza A Virus, H1N1 Subtype</term>
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<term>Influenza, Human (pathology)</term>
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<term>Orthomyxoviridae Infections (complications)</term>
<term>Orthomyxoviridae Infections (microbiology)</term>
<term>Orthomyxoviridae Infections (pathology)</term>
<term>Pneumococcal Infections (complications)</term>
<term>Pneumococcal Infections (microbiology)</term>
<term>Pneumococcal Infections (pathology)</term>
<term>Pulmonary Embolism (microbiology)</term>
<term>Pulmonary Embolism (pathology)</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Streptococcus pneumoniae</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Co-infection ()</term>
<term>Coagulation sanguine</term>
<term>Embolie pulmonaire (anatomopathologie)</term>
<term>Embolie pulmonaire (microbiologie)</term>
<term>Femelle</term>
<term>Grippe humaine ()</term>
<term>Grippe humaine (anatomopathologie)</term>
<term>Grippe humaine (microbiologie)</term>
<term>Humains</term>
<term>Immunohistochimie</term>
<term>Infections à Orthomyxoviridae ()</term>
<term>Infections à Orthomyxoviridae (anatomopathologie)</term>
<term>Infections à Orthomyxoviridae (microbiologie)</term>
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<term>Infections à pneumocoques (anatomopathologie)</term>
<term>Infections à pneumocoques (microbiologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Pandémie de grippe de 1918-1919</term>
<term>RT-PCR</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
<term>Streptococcus pneumoniae</term>
<term>Séquençage par oligonucléotides en batterie</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Embolie pulmonaire</term>
<term>Grippe humaine</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à pneumocoques</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Coinfection</term>
<term>Influenza, Human</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumococcal Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Embolie pulmonaire</term>
<term>Grippe humaine</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à pneumocoques</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Influenza, Human</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumococcal Infections</term>
<term>Pulmonary Embolism</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Influenza, Human</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumococcal Infections</term>
<term>Pulmonary Embolism</term>
</keywords>
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<term>Blood Coagulation</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Immunohistochemistry</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza Pandemic, 1918-1919</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Streptococcus pneumoniae</term>
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<term>Co-infection</term>
<term>Coagulation sanguine</term>
<term>Femelle</term>
<term>Grippe humaine</term>
<term>Humains</term>
<term>Immunohistochimie</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à pneumocoques</term>
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<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
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<ArticleTitle>1918 pandemic influenza virus and Streptococcus pneumoniae co-infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans.</ArticleTitle>
<Pagination><MedlinePgn>85-97</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1002/path.4638</ELocationID>
<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Walters</LastName>
<ForeName>Kathie-Anne</ForeName>
<Initials>KA</Initials>
<AffiliationInfo><Affiliation>Institute for Systems Biology, Seattle, WA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>D'Agnillo</LastName>
<ForeName>Felice</ForeName>
<Initials>F</Initials>
<AffiliationInfo><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, Silver Spring, MD, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sheng</LastName>
<ForeName>Zong-Mei</ForeName>
<Initials>ZM</Initials>
<AffiliationInfo><Affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, 20892, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kindrachuk</LastName>
<ForeName>Jason</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health (NIH), Bethesda, MD, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schwartzman</LastName>
<ForeName>Louis M</ForeName>
<Initials>LM</Initials>
<AffiliationInfo><Affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, 20892, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kuestner</LastName>
<ForeName>Rolf E</ForeName>
<Initials>RE</Initials>
<AffiliationInfo><Affiliation>Institute for Systems Biology, Seattle, WA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chertow</LastName>
<ForeName>Daniel S</ForeName>
<Initials>DS</Initials>
<AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health (NIH), Bethesda, MD, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, 20892, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Golding</LastName>
<ForeName>Basil T</ForeName>
<Initials>BT</Initials>
<AffiliationInfo><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, Silver Spring, MD, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Taubenberger</LastName>
<ForeName>Jeffery K</ForeName>
<Initials>JK</Initials>
<AffiliationInfo><Affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, 20892, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kash</LastName>
<ForeName>John C</ForeName>
<Initials>JC</Initials>
<AffiliationInfo><Affiliation>Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD, 20892, USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>Z99 AI999999</GrantID>
<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>ZIA AI000986-09</GrantID>
<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>ZIA AI000995-09</GrantID>
<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType>
<PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2015</Year>
<Month>10</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Pathol</MedlineTA>
<NlmUniqueID>0204634</NlmUniqueID>
<ISSNLinking>0022-3417</ISSNLinking>
</MedlineJournalInfo>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001777" MajorTopicYN="N">Blood Coagulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D060085" MajorTopicYN="N">Coinfection</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064149" MajorTopicYN="N">Influenza Pandemic, 1918-1919</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009976" MajorTopicYN="N">Orthomyxoviridae Infections</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011008" MajorTopicYN="N">Pneumococcal Infections</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011655" MajorTopicYN="N">Pulmonary Embolism</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013296" MajorTopicYN="N">Streptococcus pneumoniae</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">1918 influenza</Keyword>
<Keyword MajorTopicYN="N">Streptococcus pneumoniae</Keyword>
<Keyword MajorTopicYN="N">co-infection</Keyword>
<Keyword MajorTopicYN="N">extrinsic pathway of coagulation</Keyword>
<Keyword MajorTopicYN="N">inflammation</Keyword>
<Keyword MajorTopicYN="N">pulmonary thrombosis</Keyword>
</KeywordList>
</MedlineCitation>
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<Day>23</Day>
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<PubMedPubDate PubStatus="revised"><Year>2015</Year>
<Month>08</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2015</Year>
<Month>09</Month>
<Day>07</Day>
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<PubMedPubDate PubStatus="entrez"><Year>2015</Year>
<Month>9</Month>
<Day>19</Day>
<Hour>6</Hour>
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<affiliations><list><country><li>États-Unis</li>
</country>
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<li>Washington (État)</li>
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<tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Walters, Kathie Anne" sort="Walters, Kathie Anne" uniqKey="Walters K" first="Kathie-Anne" last="Walters">Kathie-Anne Walters</name>
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<name sortKey="Chertow, Daniel S" sort="Chertow, Daniel S" uniqKey="Chertow D" first="Daniel S" last="Chertow">Daniel S. Chertow</name>
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<name sortKey="Kindrachuk, Jason" sort="Kindrachuk, Jason" uniqKey="Kindrachuk J" first="Jason" last="Kindrachuk">Jason Kindrachuk</name>
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