Transcriptomic Analysis Reveals a Mechanism for a Prefibrotic Phenotype in STAT1 Knockout Mice during Severe Acute Respiratory Syndrome Coronavirus Infection
Identifieur interne : 002911 ( Main/Exploration ); précédent : 002910; suivant : 002912Transcriptomic Analysis Reveals a Mechanism for a Prefibrotic Phenotype in STAT1 Knockout Mice during Severe Acute Respiratory Syndrome Coronavirus Infection
Auteurs : Gregory A. Zornetzer [États-Unis] ; Matthew B. Frieman [États-Unis] ; Elizabeth Rosenzweig [États-Unis] ; Marcus J. Korth [États-Unis] ; Carly Page [États-Unis] ; Ralph S. Baric [États-Unis] ; Michael G. Katze [États-Unis]Source :
- Journal of virology [ 0022-538X ] ; 2010.
Descripteurs français
- KwdFr :
- ARN messager (analyse), Analyse de profil d'expression de gènes, Animaux, Facteur de transcription STAT-1 (déficit), Fibrose (génétique), Fibrose (étiologie), Lymphocytes auxiliaires Th2 (immunologie), Macrophages (anatomopathologie), Maladies pulmonaires (génétique), Maladies pulmonaires (étiologie), Phénotype, Récepteur à l'interféron alpha-bêta (déficit), Souris, Souris knockout, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Virus du SRAS.
- MESH :
- analyse : ARN messager.
- anatomopathologie : Macrophages, Syndrome respiratoire aigu sévère.
- déficit : Facteur de transcription STAT-1, Récepteur à l'interféron alpha-bêta.
- génétique : Fibrose, Maladies pulmonaires.
- immunologie : Lymphocytes auxiliaires Th2, Syndrome respiratoire aigu sévère.
- étiologie : Fibrose, Maladies pulmonaires.
- Pascal (Inist)
English descriptors
- KwdEn :
- Animals, Coronavirus, Fibrosis (etiology), Fibrosis (genetics), Gene Expression Profiling, Lung Diseases (etiology), Lung Diseases (genetics), Macrophages (pathology), Mechanism, Mice, Mice, Knockout, Mouse, Phenotype, RNA, Messenger (analysis), Receptor, Interferon alpha-beta (deficiency), SARS Virus, STAT1 Transcription Factor (deficiency), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe acute respiratory syndrome, Th2 Cells (immunology).
- MESH :
- chemical , analysis : RNA, Messenger.
- chemical , deficiency : Receptor, Interferon alpha-beta, STAT1 Transcription Factor.
- etiology : Fibrosis, Lung Diseases.
- genetics : Fibrosis, Lung Diseases.
- immunology : Severe Acute Respiratory Syndrome, Th2 Cells.
- pathology : Macrophages, Severe Acute Respiratory Syndrome.
- Animals, Gene Expression Profiling, Mice, Mice, Knockout, Phenotype, SARS Virus.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) infection can cause the development of severe end-stage lung disease characterized by acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. The mechanisms by which pulmonary lesions and fibrosis are generated during SARS-CoV infection are not known. Using high-throughput mRNA profiling, we examined the transcriptional response of wild-type (WT), type I interferon receptor knockout (IFNAR1-/-), and STAT1 knockout (STAT1-/-) mice infected with a recombinant mouse-adapted SARS-CoV (rMA15) to better understand the contribution of specific gene expression changes to disease progression. Despite a deletion of the type I interferon receptor, strong expression of interferon-stimulated genes was observed in the lungs of IFNAR1-/- mice, contributing to clearance of the virus. In contrast, STAT1-/- mice exhibited a defect in the expression of interferon-stimulated genes and were unable to clear the infection, resulting in a lethal outcome. STAT1-/- mice exhibited dysregulation of T-cell and macrophage differentiation, leading to a TH2-biased immune response and the development of alternatively activated macrophages that mediate a profibrotic environment within the lung. We propose that a combination of impaired viral clearance and T-cell/macrophage dysregulation causes the formation of prefibrotic lesions in the lungs of rMA15-infected STAT1-/- mice.
Url:
Affiliations:
- États-Unis
- Caroline du Nord, Maryland, Washington (État)
- Chapel Hill (Caroline du Nord), College Park (Maryland), Seattle
- Université de Caroline du Nord à Chapel Hill, Université de Washington, Université du Maryland
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Le document en format XML
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Frieman</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Microbiology and Immunology, University of Maryland</s1><s2>Baltimore, Maryland 21202</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">College Park (Maryland)</settlement><region type="state">Maryland</region></placeName><orgName type="university">Université du Maryland</orgName></affiliation></author><author><name sortKey="Rosenzweig, Elizabeth" sort="Rosenzweig, Elizabeth" uniqKey="Rosenzweig E" first="Elizabeth" last="Rosenzweig">Elizabeth Rosenzweig</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Microbiology, School of Medicine, University of Washington</s1><s2>Seattle, Washington 98195</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Korth, Marcus J" sort="Korth, Marcus J" uniqKey="Korth M" first="Marcus J." last="Korth">Marcus J. Korth</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Microbiology, School of Medicine, University of Washington</s1><s2>Seattle, Washington 98195</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Page, Carly" sort="Page, Carly" uniqKey="Page C" first="Carly" last="Page">Carly Page</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Microbiology and Immunology, University of Maryland</s1><s2>Baltimore, Maryland 21202</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">College Park (Maryland)</settlement><region type="state">Maryland</region></placeName><orgName type="university">Université du Maryland</orgName></affiliation></author><author><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S." last="Baric">Ralph S. Baric</name><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>Department of Epidemiology, University of North Carolina at Chapel Hill</s1><s2>Chapel Hill, North Carolina 27599</s2><s3>USA</s3><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Chapel Hill (Caroline du Nord)</settlement><region type="state">Caroline du Nord</region></placeName><orgName type="university">Université de Caroline du Nord à Chapel Hill</orgName></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 wicri:level="4"><inist:fA14 i1="01"><s1>Department of Microbiology, School of Medicine, University of Washington</s1><s2>Seattle, Washington 98195</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName><orgName type="university">Université de Washington</orgName></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Coronavirus</term><term>Fibrosis (etiology)</term><term>Fibrosis (genetics)</term><term>Gene Expression Profiling</term><term>Lung Diseases (etiology)</term><term>Lung Diseases (genetics)</term><term>Macrophages (pathology)</term><term>Mechanism</term><term>Mice</term><term>Mice, Knockout</term><term>Mouse</term><term>Phenotype</term><term>RNA, Messenger (analysis)</term><term>Receptor, Interferon alpha-beta (deficiency)</term><term>SARS Virus</term><term>STAT1 Transcription Factor (deficiency)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Severe acute respiratory syndrome</term><term>Th2 Cells (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (analyse)</term><term>Analyse de profil d'expression de gènes</term><term>Animaux</term><term>Facteur de transcription STAT-1 (déficit)</term><term>Fibrose (génétique)</term><term>Fibrose (étiologie)</term><term>Lymphocytes auxiliaires Th2 (immunologie)</term><term>Macrophages (anatomopathologie)</term><term>Maladies pulmonaires (génétique)</term><term>Maladies pulmonaires (étiologie)</term><term>Phénotype</term><term>Récepteur à l'interféron alpha-bêta (déficit)</term><term>Souris</term><term>Souris knockout</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptor, Interferon alpha-beta</term><term>STAT1 Transcription Factor</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>ARN messager</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Macrophages</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Facteur de transcription STAT-1</term><term>Récepteur à l'interféron alpha-bêta</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Fibrosis</term><term>Lung Diseases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Fibrosis</term><term>Lung Diseases</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Fibrose</term><term>Maladies pulmonaires</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes auxiliaires Th2</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Macrophages</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Fibrose</term><term>Maladies pulmonaires</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression Profiling</term><term>Mice</term><term>Mice, Knockout</term><term>Phenotype</term><term>SARS Virus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Animaux</term><term>Phénotype</term><term>Souris</term><term>Coronavirus</term><term>Mécanisme</term><term>Phénotype</term><term>Souris knockout</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) infection can cause the development of severe end-stage lung disease characterized by acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. The mechanisms by which pulmonary lesions and fibrosis are generated during SARS-CoV infection are not known. Using high-throughput mRNA profiling, we examined the transcriptional response of wild-type (WT), type I interferon receptor knockout (IFNAR1<sup>-/-</sup>), and STAT1 knockout (STAT1<sup>-/-</sup>) mice infected with a recombinant mouse-adapted SARS-CoV (rMA15) to better understand the contribution of specific gene expression changes to disease progression. Despite a deletion of the type I interferon receptor, strong expression of interferon-stimulated genes was observed in the lungs of IFNAR1<sup>-/-</sup> mice, contributing to clearance of the virus. In contrast, STAT1<sup>-/-</sup> mice exhibited a defect in the expression of interferon-stimulated genes and were unable to clear the infection, resulting in a lethal outcome. STAT1<sup>-/-</sup> mice exhibited dysregulation of T-cell and macrophage differentiation, leading to a T<sub>H</sub>2-biased immune response and the development of alternatively activated macrophages that mediate a profibrotic environment within the lung. We propose that a combination of impaired viral clearance and T-cell/macrophage dysregulation causes the formation of prefibrotic lesions in the lungs of rMA15-infected STAT1<sup>-/-</sup> mice.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Caroline du Nord</li><li>Maryland</li><li>Washington (État)</li></region><settlement><li>Chapel Hill (Caroline du Nord)</li><li>College Park (Maryland)</li><li>Seattle</li></settlement><orgName><li>Université de Caroline du Nord à Chapel Hill</li><li>Université de Washington</li><li>Université du Maryland</li></orgName></list><tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Zornetzer, Gregory A" sort="Zornetzer, Gregory A" uniqKey="Zornetzer G" first="Gregory A." last="Zornetzer">Gregory A. Zornetzer</name></region><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S." last="Baric">Ralph S. Baric</name><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B." last="Frieman">Matthew B. Frieman</name><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G." last="Katze">Michael G. Katze</name><name sortKey="Korth, Marcus J" sort="Korth, Marcus J" uniqKey="Korth M" first="Marcus J." last="Korth">Marcus J. Korth</name><name sortKey="Page, Carly" sort="Page, Carly" uniqKey="Page C" first="Carly" last="Page">Carly Page</name><name sortKey="Rosenzweig, Elizabeth" sort="Rosenzweig, Elizabeth" uniqKey="Rosenzweig E" first="Elizabeth" last="Rosenzweig">Elizabeth Rosenzweig</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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