Transcriptomic analysis reveals a mechanism for a prefibrotic phenotype in STAT1 knockout mice during severe acute respiratory syndrome coronavirus infection.
Identifieur interne : 001562 ( PubMed/Checkpoint ); précédent : 001561; suivant : 001563Transcriptomic 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 ; Elizabeth Rosenzweig ; Marcus J. Korth ; Carly Page ; Ralph S. Baric ; Michael G. KatzeSource :
- Journal of virology [ 1098-5514 ] ; 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.
- Analyse de profil d'expression de gènes, Animaux, Phénotype, Souris, Souris knockout, Virus du SRAS.
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
Affiliations:
Links toward previous steps (curation, corpus...)
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pubmed:20702617Le document en format XML
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<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>
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