Accumulation of CD11b+Gr-1+cells in the lung, blood and bone marrow of mice infected with highly pathogenic H5N1 and H1N1 influenza viruses
Identifieur interne : 001830 ( Istex/Corpus ); précédent : 001829; suivant : 001831Accumulation of CD11b+Gr-1+cells in the lung, blood and bone marrow of mice infected with highly pathogenic H5N1 and H1N1 influenza viruses
Auteurs : James P. Long ; Mark S. Kotur ; Gregory V. Stark ; Richard L. Warren ; Manjula Kasoji ; Jeremy L. Craft ; Randy A. Albrecht ; Adolfo García-Sastre ; Michael G. Katze ; Katrina M. Waters ; Daphne Vasconcelos ; Patrick J. Sabourin ; Herbert S. Bresler ; Carol L. SabourinSource :
- Archives of Virology [ 0304-8608 ] ; 2013.
Abstract
Abstract: Infection with pathogenic influenza viruses is associated with intense inflammatory disease. Here, we investigated the innate immune response in mice infected with H5N1 A/Vietnam/1203/04 and with reassortant human H1N1 A/Texas/36/91 viruses containing the virulence genes hemagglutinin (HA), neuraminidase (NA) and NS1 of the 1918 pandemic virus. Inclusion of the 1918 HA and NA glycoproteins rendered a seasonal H1N1 virus capable of inducing an exacerbated host innate immune response similar to that observed for highly pathogenic A/Vietnam/1203/04 virus. Infection with 1918 HA/NA:Tx/91 and A/Vietnam/1203/04 were associated with severe lung pathology, increased cytokine and chemokine production, and significant immune cell changes, including the presence of CD11b+Gr-1+ cells in the blood, lung and bone marrow. Significant differential gene expression in the lung included pathways for cell death, apoptosis, production and response to reactive oxygen radicals, as well as arginine and proline metabolism and chemokines associated with monocyte and neutrophil/granulocyte accumulation and/or activation. Arginase was produced in the lung of animals infected with A/Vietnam/1204. These results demonstrate that the innate immune cell response results in the accumulation of CD11b+Gr-1+ cells and products that have previously been shown to contribute to T cell suppression.
Url:
DOI: 10.1007/s00705-012-1593-3
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Long</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: longj@battelle.org</mods:affiliation></affiliation></author><author><name sortKey="Kotur, Mark S" sort="Kotur, Mark S" uniqKey="Kotur M" first="Mark S." last="Kotur">Mark S. Kotur</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Stark, Gregory V" sort="Stark, Gregory V" uniqKey="Stark G" first="Gregory V." last="Stark">Gregory V. Stark</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Warren, Richard L" sort="Warren, Richard L" uniqKey="Warren R" first="Richard L." last="Warren">Richard L. Warren</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Kasoji, Manjula" sort="Kasoji, Manjula" uniqKey="Kasoji M" first="Manjula" last="Kasoji">Manjula Kasoji</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Craft, Jeremy L" sort="Craft, Jeremy L" uniqKey="Craft J" first="Jeremy L." last="Craft">Jeremy L. Craft</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Albrecht, Randy A" sort="Albrecht, Randy A" uniqKey="Albrecht R" first="Randy A." last="Albrecht">Randy A. Albrecht</name><affiliation><mods:affiliation>Department of Microbiology, Mount Sinai School of Medicine, New York, NY, USA</mods:affiliation></affiliation></author><author><name sortKey="Garcia Sastre, Adolfo" sort="Garcia Sastre, Adolfo" uniqKey="Garcia Sastre A" first="Adolfo" last="García-Sastre">Adolfo García-Sastre</name><affiliation><mods:affiliation>Department of Microbiology, Mount Sinai School of Medicine, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY, USA</mods:affiliation></affiliation></author><author><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G." last="Katze">Michael G. Katze</name><affiliation><mods:affiliation>Department of Microbiology, University of Washington, Seattle, WA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Washington National Primate Research Center, University of Washington, Seattle, WA, USA</mods:affiliation></affiliation></author><author><name sortKey="Waters, Katrina M" sort="Waters, Katrina M" uniqKey="Waters K" first="Katrina M." last="Waters">Katrina M. Waters</name><affiliation><mods:affiliation>Pacific Northwest National Laboratory, Computational Biology and Bioinformatics, Richland, WA, USA</mods:affiliation></affiliation></author><author><name sortKey="Vasconcelos, Daphne" sort="Vasconcelos, Daphne" uniqKey="Vasconcelos D" first="Daphne" last="Vasconcelos">Daphne Vasconcelos</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Sabourin, Patrick J" sort="Sabourin, Patrick J" uniqKey="Sabourin P" first="Patrick J." last="Sabourin">Patrick J. Sabourin</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Bresler, Herbert S" sort="Bresler, Herbert S" uniqKey="Bresler H" first="Herbert S." last="Bresler">Herbert S. Bresler</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author><author><name sortKey="Sabourin, Carol L" sort="Sabourin, Carol L" uniqKey="Sabourin C" first="Carol L." last="Sabourin">Carol L. Sabourin</name><affiliation><mods:affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Archives of Virology</title><title level="j" type="abbrev">Arch Virol</title><idno type="ISSN">0304-8608</idno><idno type="eISSN">1432-8798</idno><imprint><publisher ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-SWLMH5L1-1">Springer Vienna</publisher><pubPlace>Vienna</pubPlace><date type="published" when="2013">2013</date><biblScope unit="vol" from="158" to="158">158</biblScope><biblScope unit="issue" from="6" to="6">6</biblScope><biblScope unit="page" from="1305">1305</biblScope><biblScope unit="page" to="1322">1322</biblScope></imprint><idno type="ISSN">0304-8608</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0304-8608</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Infection with pathogenic influenza viruses is associated with intense inflammatory disease. Here, we investigated the innate immune response in mice infected with H5N1 A/Vietnam/1203/04 and with reassortant human H1N1 A/Texas/36/91 viruses containing the virulence genes hemagglutinin (HA), neuraminidase (NA) and NS1 of the 1918 pandemic virus. Inclusion of the 1918 HA and NA glycoproteins rendered a seasonal H1N1 virus capable of inducing an exacerbated host innate immune response similar to that observed for highly pathogenic A/Vietnam/1203/04 virus. Infection with 1918 HA/NA:Tx/91 and A/Vietnam/1203/04 were associated with severe lung pathology, increased cytokine and chemokine production, and significant immune cell changes, including the presence of CD11b+Gr-1+ cells in the blood, lung and bone marrow. Significant differential gene expression in the lung included pathways for cell death, apoptosis, production and response to reactive oxygen radicals, as well as arginine and proline metabolism and chemokines associated with monocyte and neutrophil/granulocyte accumulation and/or activation. Arginase was produced in the lung of animals infected with A/Vietnam/1204. These results demonstrate that the innate immune cell response results in the accumulation of CD11b+Gr-1+ cells and products that have previously been shown to contribute to T cell suppression.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>James P. Long</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string><json:string>E-mail: longj@battelle.org</json:string></affiliations></json:item><json:item><name>Mark S. Kotur</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Gregory V. Stark</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Richard L. Warren</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Manjula Kasoji</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Jeremy L. Craft</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Randy A. Albrecht</name><affiliations><json:string>Department of Microbiology, Mount Sinai School of Medicine, New York, NY, USA</json:string></affiliations></json:item><json:item><name>Adolfo García-Sastre</name><affiliations><json:string>Department of Microbiology, Mount Sinai School of Medicine, New York, NY, USA</json:string><json:string>Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine, New York, NY, USA</json:string><json:string>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY, USA</json:string></affiliations></json:item><json:item><name>Michael G. Katze</name><affiliations><json:string>Department of Microbiology, University of Washington, Seattle, WA, USA</json:string><json:string>Washington National Primate Research Center, University of Washington, Seattle, WA, USA</json:string></affiliations></json:item><json:item><name>Katrina M. Waters</name><affiliations><json:string>Pacific Northwest National Laboratory, Computational Biology and Bioinformatics, Richland, WA, USA</json:string></affiliations></json:item><json:item><name>Daphne Vasconcelos</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Patrick J. Sabourin</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Herbert S. Bresler</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item><json:item><name>Carol L. Sabourin</name><affiliations><json:string>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</json:string></affiliations></json:item></author><articleId><json:string>1593</json:string><json:string>s00705-012-1593-3</json:string></articleId><arkIstex>ark:/67375/VQC-3B8SKXHP-W</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>OriginalPaper</json:string></originalGenre><abstract>Abstract: Infection with pathogenic influenza viruses is associated with intense inflammatory disease. Here, we investigated the innate immune response in mice infected with H5N1 A/Vietnam/1203/04 and with reassortant human H1N1 A/Texas/36/91 viruses containing the virulence genes hemagglutinin (HA), neuraminidase (NA) and NS1 of the 1918 pandemic virus. Inclusion of the 1918 HA and NA glycoproteins rendered a seasonal H1N1 virus capable of inducing an exacerbated host innate immune response similar to that observed for highly pathogenic A/Vietnam/1203/04 virus. Infection with 1918 HA/NA:Tx/91 and A/Vietnam/1203/04 were associated with severe lung pathology, increased cytokine and chemokine production, and significant immune cell changes, including the presence of CD11b+Gr-1+ cells in the blood, lung and bone marrow. Significant differential gene expression in the lung included pathways for cell death, apoptosis, production and response to reactive oxygen radicals, as well as arginine and proline metabolism and chemokines associated with monocyte and neutrophil/granulocyte accumulation and/or activation. Arginase was produced in the lung of animals infected with A/Vietnam/1204. These results demonstrate that the innate immune cell response results in the accumulation of CD11b+Gr-1+ cells and products that have previously been shown to contribute to T cell suppression.</abstract><qualityIndicators><score>7.947</score><pdfWordCount>9653</pdfWordCount><pdfCharCount>61755</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>18</pdfPageCount><pdfPageSize>595.276 x 790.866 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>190</abstractWordCount><abstractCharCount>1390</abstractCharCount><keywordCount>0</keywordCount><pdfWordsPerPage>536</pdfWordsPerPage><pdfText>true</pdfText></qualityIndicators><title>Accumulation of CD11b+Gr-1+cells in the lung, blood and bone marrow of mice infected with highly pathogenic H5N1 and H1N1 influenza viruses</title><genre><json:string>article</json:string></genre><host><title>Archives of 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highly pathogenic H5N1 and H1N1 influenza viruses</title><author role="corresp"><persName><forename type="first">James</forename><forename type="middle">P.</forename><surname>Long</surname></persName><email>longj@battelle.org</email><affiliation><orgName type="institution">Battelle</orgName><address><street>505 King Avenue</street><settlement>Columbus</settlement><region>OH</region><postCode>43201</postCode><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation></author><author><persName><forename type="first">Mark</forename><forename type="middle">S.</forename><surname>Kotur</surname></persName><affiliation><orgName type="institution">Battelle</orgName><address><street>505 King Avenue</street><settlement>Columbus</settlement><region>OH</region><postCode>43201</postCode><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation></author><author><persName><forename type="first">Gregory</forename><forename type="middle">V.</forename><surname>Stark</surname></persName><affiliation><orgName type="institution">Battelle</orgName><address><street>505 King Avenue</street><settlement>Columbus</settlement><region>OH</region><postCode>43201</postCode><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation></author><author><persName><forename type="first">Richard</forename><forename type="middle">L.</forename><surname>Warren</surname></persName><affiliation><orgName type="institution">Battelle</orgName><address><street>505 King Avenue</street><settlement>Columbus</settlement><region>OH</region><postCode>43201</postCode><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation></author><author><persName><forename type="first">Manjula</forename><surname>Kasoji</surname></persName><affiliation><orgName type="institution">Battelle</orgName><address><street>505 King Avenue</street><settlement>Columbus</settlement><region>OH</region><postCode>43201</postCode><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation></author><author><persName><forename type="first">Jeremy</forename><forename type="middle">L.</forename><surname>Craft</surname></persName><affiliation><orgName type="institution">Battelle</orgName><address><street>505 King Avenue</street><settlement>Columbus</settlement><region>OH</region><postCode>43201</postCode><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation></author><author><persName><forename type="first">Randy</forename><forename type="middle">A.</forename><surname>Albrecht</surname></persName><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="institution">Mount Sinai School of Medicine</orgName><address><settlement>New York</settlement><region>NY</region><country key="US" xml:lang="en">UNITED 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STATES</country></address></affiliation></author><author><persName><forename type="first">Michael</forename><forename type="middle">G.</forename><surname>Katze</surname></persName><affiliation><orgName type="department">Department of Microbiology</orgName><orgName type="institution">University of Washington</orgName><address><settlement>Seattle</settlement><region>WA</region><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation><affiliation><orgName type="institution">Washington National Primate Research Center, University of Washington</orgName><address><settlement>Seattle</settlement><region>WA</region><country key="US" xml:lang="en">UNITED STATES</country></address></affiliation></author><author><persName><forename type="first">Katrina</forename><forename type="middle">M.</forename><surname>Waters</surname></persName><affiliation><orgName type="department">Pacific Northwest National Laboratory</orgName><orgName type="institution">Computational Biology and 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type="article-id">1593</idno></analytic><monogr><title level="j" type="main">Archives of Virology</title><title level="j" type="abbrev">Arch Virol</title><idno type="journal-id">705</idno><idno type="pISSN">0304-8608</idno><idno type="eISSN">1432-8798</idno><imprint><publisher ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-SWLMH5L1-1">Springer Vienna</publisher><pubPlace>Vienna</pubPlace><date type="published" when="2013">2013</date><biblScope unit="vol" from="158" to="158">158</biblScope><biblScope unit="issue" from="6" to="6">6</biblScope><biblScope unit="page" from="1305">1305</biblScope><biblScope unit="page" to="1322">1322</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.48" when="2020-05-28"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various 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Infection with 1918 HA/NA:Tx/91 and A/Vietnam/1203/04 were associated with severe lung pathology, increased cytokine and chemokine production, and significant immune cell changes, including the presence of CD11b<hi rend="superscript">+</hi>Gr-1<hi rend="superscript">+</hi> cells in the blood, lung and bone marrow. Significant differential gene expression in the lung included pathways for cell death, apoptosis, production and response to reactive oxygen radicals, as well as arginine and proline metabolism and chemokines associated with monocyte and neutrophil/granulocyte accumulation and/or activation. Arginase was produced in the lung of animals infected with A/Vietnam/1204. These results demonstrate that the innate immune cell response results in the accumulation of CD11b<hi rend="superscript">+</hi>Gr-1<hi rend="superscript">+</hi> cells and products that have previously been shown to contribute to T cell suppression.</p></abstract><textClass ana="subject"><keywords scheme="journal-subject"><list><item><label>SCB</label><term type="Primary">Biomedicine</term></item><item><label>SCB22003</label><term type="Secondary" subtype="priority-1">Virology</term></item><item><label>SCB16003</label><term type="Secondary" subtype="priority-2">Medical Microbiology</term></item><item><label>SCH33096</label><term type="Secondary" subtype="priority-3">Infectious Diseases</term></item></list></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2020-05-28" who="#istex" xml:id="pub2tei">formatting</change><change when="2012-12-21">Registration</change><change when="2012-05-17">Received</change><change 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VolumeType="Regular"><VolumeIDStart>158</VolumeIDStart><VolumeIDEnd>158</VolumeIDEnd><VolumeIssueCount>12</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular" OutputMedium="All"><IssueInfo IssueType="Regular" TocLevels="0"><IssueIDStart>6</IssueIDStart><IssueIDEnd>6</IssueIDEnd><IssueArticleCount>35</IssueArticleCount><IssueHistory><OnlineDate><Year>2013</Year><Month>5</Month><Day>31</Day></OnlineDate><PrintDate><Year>2013</Year><Month>5</Month><Day>30</Day></PrintDate><CoverDate><Year>2013</Year><Month>6</Month></CoverDate><PricelistYear>2013</PricelistYear></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag Wien</CopyrightHolderName><CopyrightYear>2013</CopyrightYear></IssueCopyright></IssueInfo><Article ID="s00705-012-1593-3" OutputMedium="All"><ArticleInfo ArticleType="OriginalPaper" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>1593</ArticleID><ArticleDOI>10.1007/s00705-012-1593-3</ArticleDOI><ArticleSequenceNumber>19</ArticleSequenceNumber><ArticleTitle Language="En" OutputMedium="All">Accumulation of CD11b<Superscript>+</Superscript>Gr-1<Superscript>+</Superscript> cells in the lung, blood and bone marrow of mice infected with highly pathogenic H5N1 and H1N1 influenza viruses</ArticleTitle><ArticleCategory>Original Article</ArticleCategory><ArticleFirstPage>1305</ArticleFirstPage><ArticleLastPage>1322</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2012</Year><Month>12</Month><Day>21</Day></RegistrationDate><Received><Year>2012</Year><Month>5</Month><Day>17</Day></Received><Accepted><Year>2012</Year><Month>10</Month><Day>26</Day></Accepted><OnlineDate><Year>2013</Year><Month>2</Month><Day>9</Day></OnlineDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag Wien</CopyrightHolderName><CopyrightYear>2013</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>James</GivenName><GivenName>P.</GivenName><FamilyName>Long</FamilyName></AuthorName><Contact><Phone>+614-424-4399</Phone><Fax>+614-458-4399</Fax><Email>longj@battelle.org</Email></Contact></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Mark</GivenName><GivenName>S.</GivenName><FamilyName>Kotur</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Gregory</GivenName><GivenName>V.</GivenName><FamilyName>Stark</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Richard</GivenName><GivenName>L.</GivenName><FamilyName>Warren</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Manjula</GivenName><FamilyName>Kasoji</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Jeremy</GivenName><GivenName>L.</GivenName><FamilyName>Craft</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Randy</GivenName><GivenName>A.</GivenName><FamilyName>Albrecht</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2 Aff3 Aff4"><AuthorName DisplayOrder="Western"><GivenName>Adolfo</GivenName><FamilyName>García-Sastre</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff5 Aff6"><AuthorName DisplayOrder="Western"><GivenName>Michael</GivenName><GivenName>G.</GivenName><FamilyName>Katze</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff7"><AuthorName DisplayOrder="Western"><GivenName>Katrina</GivenName><GivenName>M.</GivenName><FamilyName>Waters</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Daphne</GivenName><FamilyName>Vasconcelos</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Patrick</GivenName><GivenName>J.</GivenName><FamilyName>Sabourin</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Herbert</GivenName><GivenName>S.</GivenName><FamilyName>Bresler</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Carol</GivenName><GivenName>L.</GivenName><FamilyName>Sabourin</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgName>Battelle</OrgName><OrgAddress><Street>505 King Avenue</Street><City>Columbus</City><State>OH</State><Postcode>43201</Postcode><Country Code="US">USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Microbiology</OrgDivision><OrgName>Mount Sinai School of Medicine</OrgName><OrgAddress><City>New York</City><State>NY</State><Country Code="US">USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Medicine, Division of Infectious Diseases</OrgDivision><OrgName>Mount Sinai School of Medicine</OrgName><OrgAddress><City>New York</City><State>NY</State><Country Code="US">USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgName>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine</OrgName><OrgAddress><City>New York</City><State>NY</State><Country Code="US">USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff5"><OrgDivision>Department of Microbiology</OrgDivision><OrgName>University of Washington</OrgName><OrgAddress><City>Seattle</City><State>WA</State><Country Code="US">USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff6"><OrgName>Washington National Primate Research Center, University of Washington</OrgName><OrgAddress><City>Seattle</City><State>WA</State><Country Code="US">USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff7"><OrgDivision>Pacific Northwest National Laboratory</OrgDivision><OrgName>Computational Biology and Bioinformatics</OrgName><OrgAddress><City>Richland</City><State>WA</State><Country Code="US">USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En" OutputMedium="All"><Heading>Abstract</Heading><Para>Infection with pathogenic influenza viruses is associated with intense inflammatory disease. Here, we investigated the innate immune response in mice infected with H5N1 A/Vietnam/1203/04 and with reassortant human H1N1 A/Texas/36/91 viruses containing the virulence genes hemagglutinin (HA), neuraminidase (NA) and NS1 of the 1918 pandemic virus. Inclusion of the 1918 HA and NA glycoproteins rendered a seasonal H1N1 virus capable of inducing an exacerbated host innate immune response similar to that observed for highly pathogenic A/Vietnam/1203/04 virus. Infection with 1918 HA/NA:Tx/91 and A/Vietnam/1203/04 were associated with severe lung pathology, increased cytokine and chemokine production, and significant immune cell changes, including the presence of CD11b<Superscript>+</Superscript>Gr-1<Superscript>+</Superscript> cells in the blood, lung and bone marrow. Significant differential gene expression in the lung included pathways for cell death, apoptosis, production and response to reactive oxygen radicals, as well as arginine and proline metabolism and chemokines associated with monocyte and neutrophil/granulocyte accumulation and/or activation. Arginase was produced in the lung of animals infected with A/Vietnam/1204. These results demonstrate that the innate immune cell response results in the accumulation of CD11b<Superscript>+</Superscript>Gr-1<Superscript>+</Superscript> cells and products that have previously been shown to contribute to T cell suppression.</Para></Abstract></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Accumulation of CD11b+Gr-1+cells in the lung, blood and bone marrow of mice infected with highly pathogenic H5N1 and H1N1 influenza viruses</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Accumulation of CD11b+Gr-1+cells in the lung, blood and bone marrow of mice infected with highly pathogenic H5N1 and H1N1 influenza viruses</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">James</namePart><namePart type="given">P.</namePart><namePart type="family">Long</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><affiliation>E-mail: longj@battelle.org</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="given">S.</namePart><namePart type="family">Kotur</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregory</namePart><namePart type="given">V.</namePart><namePart type="family">Stark</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard</namePart><namePart type="given">L.</namePart><namePart type="family">Warren</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Manjula</namePart><namePart type="family">Kasoji</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeremy</namePart><namePart type="given">L.</namePart><namePart type="family">Craft</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Randy</namePart><namePart type="given">A.</namePart><namePart type="family">Albrecht</namePart><affiliation>Department of Microbiology, Mount Sinai School of Medicine, New York, NY, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Adolfo</namePart><namePart type="family">García-Sastre</namePart><affiliation>Department of Microbiology, Mount Sinai School of Medicine, New York, NY, USA</affiliation><affiliation>Department of Medicine, Division of Infectious Diseases, Mount Sinai School of Medicine, New York, NY, USA</affiliation><affiliation>Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="given">G.</namePart><namePart type="family">Katze</namePart><affiliation>Department of Microbiology, University of Washington, Seattle, WA, USA</affiliation><affiliation>Washington National Primate Research Center, University of Washington, Seattle, WA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katrina</namePart><namePart type="given">M.</namePart><namePart type="family">Waters</namePart><affiliation>Pacific Northwest National Laboratory, Computational Biology and Bioinformatics, Richland, WA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daphne</namePart><namePart type="family">Vasconcelos</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patrick</namePart><namePart type="given">J.</namePart><namePart type="family">Sabourin</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Herbert</namePart><namePart type="given">S.</namePart><namePart type="family">Bresler</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carol</namePart><namePart type="given">L.</namePart><namePart type="family">Sabourin</namePart><affiliation>Battelle, 505 King Avenue, 43201, Columbus, OH, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Springer Vienna</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">2012-05-17</dateCreated><dateIssued encoding="w3cdtf">2013-06-01</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Infection with pathogenic influenza viruses is associated with intense inflammatory disease. Here, we investigated the innate immune response in mice infected with H5N1 A/Vietnam/1203/04 and with reassortant human H1N1 A/Texas/36/91 viruses containing the virulence genes hemagglutinin (HA), neuraminidase (NA) and NS1 of the 1918 pandemic virus. Inclusion of the 1918 HA and NA glycoproteins rendered a seasonal H1N1 virus capable of inducing an exacerbated host innate immune response similar to that observed for highly pathogenic A/Vietnam/1203/04 virus. Infection with 1918 HA/NA:Tx/91 and A/Vietnam/1203/04 were associated with severe lung pathology, increased cytokine and chemokine production, and significant immune cell changes, including the presence of CD11b+Gr-1+ cells in the blood, lung and bone marrow. Significant differential gene expression in the lung included pathways for cell death, apoptosis, production and response to reactive oxygen radicals, as well as arginine and proline metabolism and chemokines associated with monocyte and neutrophil/granulocyte accumulation and/or activation. Arginase was produced in the lung of animals infected with A/Vietnam/1204. These results demonstrate that the innate immune cell response results in the accumulation of CD11b+Gr-1+ cells and products that have previously been shown to contribute to T cell suppression.</abstract><note>Original Article</note><relatedItem type="host"><titleInfo><title>Archives of Virology</title><subTitle>Official Journal of the Virology Division of the International Union of Microbiological Societies</subTitle></titleInfo><titleInfo type="abbreviated"><title>Arch Virol</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">2013</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><subject><genre>Journal-Subject-Collection</genre><topic authority="SpringerSubjectCodes" authorityURI="SC3">Biomedical and Life Sciences</topic></subject><classification authority="Journal-SubjectCollection-Code">SC3</classification><subject><genre>Journal-Subject-Group</genre><topic authority="SpringerSubjectCodes" authorityURI="SCB">Biomedicine</topic><topic authority="SpringerSubjectCodes" authorityURI="SCB22003">Virology</topic><topic authority="SpringerSubjectCodes" authorityURI="SCB16003">Medical Microbiology</topic><topic authority="SpringerSubjectCodes" authorityURI="SCH33096">Infectious Diseases</topic></subject><identifier type="ISSN">0304-8608</identifier><identifier type="eISSN">1432-8798</identifier><identifier type="JournalID">705</identifier><identifier type="IssueArticleCount">35</identifier><identifier type="VolumeIssueCount">12</identifier><part><date>2013</date><detail type="volume"><number>158</number><caption>vol.</caption></detail><detail type="issue"><number>6</number><caption>no.</caption></detail><extent unit="pages"><start>1305</start><end>1322</end></extent></part><recordInfo><recordOrigin>Springer-Verlag Wien, 2013</recordOrigin></recordInfo></relatedItem><identifier type="istex">1F236A1DA61066444ABF28C548D5704A6A28E7C0</identifier><identifier type="ark">ark:/67375/VQC-3B8SKXHP-W</identifier><identifier type="DOI">10.1007/s00705-012-1593-3</identifier><identifier type="ArticleID">1593</identifier><identifier type="ArticleID">s00705-012-1593-3</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag Wien, 2013</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Converted from (version 1.2.14) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2020-05-28</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-3B8SKXHP-W/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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