Induction of alternatively activated macrophages enhances pathogenesis during severe acute respiratory syndrome coronavirus infection.
Identifieur interne : 002568 ( Ncbi/Curation ); précédent : 002567; suivant : 002569Induction of alternatively activated macrophages enhances pathogenesis during severe acute respiratory syndrome coronavirus infection.
Auteurs : Carly Page [États-Unis] ; Lindsay Goicochea ; Krystal Matthews ; Yong Zhang ; Peter Klover ; Michael J. Holtzman ; Lothar Hennighausen ; Matthew FriemanSource :
- Journal of virology [ 1098-5514 ] ; 2012.
Descripteurs français
- KwdFr :
- Activation des macrophages, Amorces ADN, Animaux, Facteur de transcription STAT-1 (génétique), Facteur de transcription STAT-1 (physiologie), Immunohistochimie, Macrophages péritonéaux (immunologie), Souris, Souris de lignée C57BL, Souris knockout, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Séquence nucléotidique, Virus du SRAS (isolement et purification).
- MESH :
- génétique : Facteur de transcription STAT-1.
- immunologie : Macrophages péritonéaux, Syndrome respiratoire aigu sévère.
- isolement et purification : Virus du SRAS.
- physiologie : Facteur de transcription STAT-1.
- virologie : Syndrome respiratoire aigu sévère.
- Activation des macrophages, Amorces ADN, Animaux, Immunohistochimie, Souris, Souris de lignée C57BL, Souris knockout, Séquence nucléotidique.
English descriptors
- KwdEn :
- Animals, Base Sequence, DNA Primers, Immunohistochemistry, Macrophage Activation, Macrophages, Peritoneal (immunology), Mice, Mice, Inbred C57BL, Mice, Knockout, SARS Virus (isolation & purification), STAT1 Transcription Factor (genetics), STAT1 Transcription Factor (physiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , genetics : STAT1 Transcription Factor.
- chemical , physiology : STAT1 Transcription Factor.
- chemical : DNA Primers.
- immunology : Macrophages, Peritoneal, Severe Acute Respiratory Syndrome.
- isolation & purification : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Base Sequence, Immunohistochemistry, Macrophage Activation, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
Infection with severe acute respiratory syndrome coronavirus (SARS-CoV) causes acute lung injury (ALI) that often leads to severe lung disease. A mouse model of acute SARS-CoV infection has been helpful in understanding the host response to infection; however, there are still unanswered questions concerning SARS-CoV pathogenesis. We have shown that STAT1 plays an important role in the severity of SARS-CoV pathogenesis and that it is independent of the role of STAT1 in interferon signaling. Mice lacking STAT1 have greater weight loss, severe lung pathology with pre-pulmonary-fibrosis-like lesions, and an altered immune response following infection with SARS-CoV. We hypothesized that STAT1 plays a role in the polarization of the immune response, specifically in macrophages, resulting in a worsened outcome. To test this, we created bone marrow chimeras and cell-type-specific knockouts of STAT1 to identify which cell type(s) is critical to protection from severe lung disease after SARS-CoV infection. Bone marrow chimera experiments demonstrated that hematopoietic cells are responsible for the pathogenesis in STAT1(-/-) mice, and because of an induction of alternatively activated (AA) macrophages after infection, we hypothesized that the AA macrophages were critical for disease severity. Mice with STAT1 in either monocytes and macrophages (LysM/STAT1) or ciliated lung epithelial cells (FoxJ1/STAT1) deleted were created. Following infection, LysM/STAT1 mice display severe lung pathology, while FoxJ1/STAT1 mice display normal lung pathology. We hypothesized that AA macrophages were responsible for this STAT1-dependent pathology and therefore created STAT1/STAT6(-/-) double-knockout mice. STAT6 is essential for the development of AA macrophages. Infection of the double-knockout mice displayed a lack of lung disease and prefibrotic lesions, suggesting that AA macrophage production may be the cause of STAT1-dependent lung disease. We propose that the control of AA macrophages by STAT1 is critical to regulating immune pathologies and for protection from long-term progression to fibrotic lung disease in a mouse model of SARS-CoV infection.
DOI: 10.1128/JVI.01689-12
PubMed: 23015710
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pubmed:23015710Le document en format XML
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<term>Macrophage Activation</term>
<term>Macrophages, Peritoneal (immunology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
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<term>Animaux</term>
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<term>Facteur de transcription STAT-1 (physiologie)</term>
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<term>Macrophages péritonéaux (immunologie)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
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<front><div type="abstract" xml:lang="en">Infection with severe acute respiratory syndrome coronavirus (SARS-CoV) causes acute lung injury (ALI) that often leads to severe lung disease. A mouse model of acute SARS-CoV infection has been helpful in understanding the host response to infection; however, there are still unanswered questions concerning SARS-CoV pathogenesis. We have shown that STAT1 plays an important role in the severity of SARS-CoV pathogenesis and that it is independent of the role of STAT1 in interferon signaling. Mice lacking STAT1 have greater weight loss, severe lung pathology with pre-pulmonary-fibrosis-like lesions, and an altered immune response following infection with SARS-CoV. We hypothesized that STAT1 plays a role in the polarization of the immune response, specifically in macrophages, resulting in a worsened outcome. To test this, we created bone marrow chimeras and cell-type-specific knockouts of STAT1 to identify which cell type(s) is critical to protection from severe lung disease after SARS-CoV infection. Bone marrow chimera experiments demonstrated that hematopoietic cells are responsible for the pathogenesis in STAT1(-/-) mice, and because of an induction of alternatively activated (AA) macrophages after infection, we hypothesized that the AA macrophages were critical for disease severity. Mice with STAT1 in either monocytes and macrophages (LysM/STAT1) or ciliated lung epithelial cells (FoxJ1/STAT1) deleted were created. Following infection, LysM/STAT1 mice display severe lung pathology, while FoxJ1/STAT1 mice display normal lung pathology. We hypothesized that AA macrophages were responsible for this STAT1-dependent pathology and therefore created STAT1/STAT6(-/-) double-knockout mice. STAT6 is essential for the development of AA macrophages. Infection of the double-knockout mice displayed a lack of lung disease and prefibrotic lesions, suggesting that AA macrophage production may be the cause of STAT1-dependent lung disease. We propose that the control of AA macrophages by STAT1 is critical to regulating immune pathologies and for protection from long-term progression to fibrotic lung disease in a mouse model of SARS-CoV infection.</div>
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