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 : 001669 ( Main/Curation ); précédent : 001668; suivant : 001670Accumulation 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 [États-Unis] ; Mark S. Kotur [États-Unis] ; Gregory V. Stark [États-Unis] ; Richard L. Warren [États-Unis] ; Manjula Kasoji [États-Unis] ; Jeremy L. Craft [États-Unis] ; Randy A. Albrecht [États-Unis] ; Adolfo García-Sastre [États-Unis] ; Michael G. Katze [États-Unis] ; Katrina M. Waters [États-Unis] ; Daphne Vasconcelos [États-Unis] ; Patrick J. Sabourin [États-Unis] ; Herbert S. Bresler [États-Unis] ; Carol L. Sabourin [États-Unis]Source :
- 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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Sabourin</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Battelle, 505 King Avenue, 43201, Columbus, OH</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></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 wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Battelle, 505 King Avenue, 43201, Columbus, OH</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></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 wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Battelle, 505 King Avenue, 43201, Columbus, OH</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></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></record>Pour manipuler ce document sous Unix (Dilib)
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