Transcriptomic analysis reveals a mechanism for a prefibrotic phenotype in STAT1 knockout mice during severe acute respiratory syndrome coronavirus infection.
Identifieur interne : 001650 ( PubMed/Corpus ); précédent : 001649; suivant : 001651Transcriptomic analysis reveals a mechanism for a prefibrotic phenotype in STAT1 knockout mice during severe acute respiratory syndrome coronavirus infection.
Auteurs : Gregory A. Zornetzer ; Matthew B. Frieman ; Elizabeth Rosenzweig ; Marcus J. Korth ; Carly Page ; Ralph S. Baric ; Michael G. KatzeSource :
- Journal of virology [ 1098-5514 ] ; 2010.
English descriptors
- KwdEn :
- Animals, Fibrosis (etiology), Fibrosis (genetics), Gene Expression Profiling, Lung Diseases (etiology), Lung Diseases (genetics), Macrophages (pathology), Mice, Mice, Knockout, 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), 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.
DOI: 10.1128/JVI.01130-10
PubMed: 20702617
Links to Exploration step
pubmed:20702617Le document en format XML
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Katze</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</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>Mice</term><term>Mice, Knockout</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>Th2 Cells (immunology)</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="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="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" 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></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-/-), 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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20702617</PMID><DateCompleted><Year>2010</Year><Month>11</Month><Day>04</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>84</Volume><Issue>21</Issue><PubDate><Year>2010</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Transcriptomic analysis reveals a mechanism for a prefibrotic phenotype in STAT1 knockout mice during severe acute respiratory syndrome coronavirus infection.</ArticleTitle><Pagination><MedlinePgn>11297-309</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.01130-10</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zornetzer</LastName><ForeName>Gregory A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Department of Microbiology, School of Medicine, University of Washington, Box 358070, Seattle, WA 98195-8070, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frieman</LastName><ForeName>Matthew B</ForeName><Initials>MB</Initials></Author><Author ValidYN="Y"><LastName>Rosenzweig</LastName><ForeName>Elizabeth</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Korth</LastName><ForeName>Marcus J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Page</LastName><ForeName>Carly</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Baric</LastName><ForeName>Ralph S</ForeName><Initials>RS</Initials></Author><Author ValidYN="Y"><LastName>Katze</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL080621</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 AI007540</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI66542</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI075297</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL080621</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI075297</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH 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