Overactive Epidermal Growth Factor Receptor Signaling Leads to Increased Fibrosis after Severe Acute Respiratory Syndrome Coronavirus Infection.
Identifieur interne : 000D93 ( Main/Exploration ); précédent : 000D92; suivant : 000D94Overactive Epidermal Growth Factor Receptor Signaling Leads to Increased Fibrosis after Severe Acute Respiratory Syndrome Coronavirus Infection.
Auteurs : Thiagarajan Venkataraman [États-Unis] ; Christopher M. Coleman [États-Unis] ; Matthew B. Frieman [États-Unis]Source :
- Journal of virology [ 1098-5514 ] ; 2017.
Descripteurs français
- KwdFr :
- Amphiréguline (administration et posologie), Amphiréguline (métabolisme), Animaux, Cicatrisation de plaie (), Fibrose pulmonaire (anatomopathologie), Fibrose pulmonaire (métabolisme), Fibrose pulmonaire (virologie), Humains, Modèles animaux de maladie humaine, Poumon (anatomopathologie), Poumon (virologie), Récepteurs ErbB (métabolisme), Souris, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Transduction du signal, Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- administration et posologie : Amphiréguline.
- anatomopathologie : Fibrose pulmonaire, Poumon, Syndrome respiratoire aigu sévère.
- métabolisme : Amphiréguline, Fibrose pulmonaire, Récepteurs ErbB, Syndrome respiratoire aigu sévère.
- pathogénicité : Virus du SRAS.
- physiologie : Virus du SRAS.
- virologie : Fibrose pulmonaire, Poumon, Syndrome respiratoire aigu sévère.
- Animaux, Cicatrisation de plaie, Humains, Modèles animaux de maladie humaine, Souris, Transduction du signal.
English descriptors
- KwdEn :
- Amphiregulin (administration & dosage), Amphiregulin (metabolism), Animals, Disease Models, Animal, ErbB Receptors (metabolism), Humans, Lung (pathology), Lung (virology), Mice, Pulmonary Fibrosis (metabolism), Pulmonary Fibrosis (pathology), Pulmonary Fibrosis (virology), SARS Virus (pathogenicity), SARS Virus (physiology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Signal Transduction, Wound Healing (drug effects).
- MESH :
- chemical , administration & dosage : Amphiregulin.
- chemical , metabolism : Amphiregulin, ErbB Receptors.
- drug effects : Wound Healing.
- metabolism : Pulmonary Fibrosis, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Lung, Pulmonary Fibrosis, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- virology : Lung, Pulmonary Fibrosis, Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Humans, Mice, Signal Transduction.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic respiratory virus that causes morbidity and mortality in humans. After infection with SARS-CoV, the acute lung injury caused by the virus must be repaired to regain lung function. A dysregulation in this wound healing process leads to fibrosis. Many survivors of SARS-CoV infection develop pulmonary fibrosis (PF), with higher prevalence in older patients. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth factor receptor (EGFR), is critical to recovery from SARS-CoV-induced tissue damage. In mice with constitutively active EGFR [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection, the EGFR ligands amphiregulin and heparin-binding EGF-like growth factor (HB-EGF) are upregulated, and exogenous addition of these ligands during infection leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses.IMPORTANCE PF has many causative triggers, including severe respiratory viruses such as SARS-CoV. Currently there are no treatments to prevent the onset or limit the progression of PF, and the molecular pathways underlying the development of PF are not well understood. In this study, we identified a role for the balanced control of EGFR signaling as a key factor in progression to PF. These data demonstrate that therapeutic treatment modulating EGFR activation could protect against PF development caused by severe respiratory virus infection.
DOI: 10.1128/JVI.00182-17
PubMed: 28404843
Affiliations:
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Coleman</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, The University of Maryland at Baltimore, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, The University of Maryland at Baltimore, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B" last="Frieman">Matthew B. Frieman</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, The University of Maryland at Baltimore, Baltimore, Maryland, USA mfrieman@som.umaryland.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, The University of Maryland at Baltimore, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amphiregulin (administration & dosage)</term><term>Amphiregulin (metabolism)</term><term>Animals</term><term>Disease Models, Animal</term><term>ErbB Receptors (metabolism)</term><term>Humans</term><term>Lung (pathology)</term><term>Lung (virology)</term><term>Mice</term><term>Pulmonary Fibrosis (metabolism)</term><term>Pulmonary Fibrosis (pathology)</term><term>Pulmonary Fibrosis (virology)</term><term>SARS Virus (pathogenicity)</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (metabolism)</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Signal Transduction</term><term>Wound Healing (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Amphiréguline (administration et posologie)</term><term>Amphiréguline (métabolisme)</term><term>Animaux</term><term>Cicatrisation de plaie ()</term><term>Fibrose pulmonaire (anatomopathologie)</term><term>Fibrose pulmonaire (métabolisme)</term><term>Fibrose pulmonaire (virologie)</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Poumon (anatomopathologie)</term><term>Poumon (virologie)</term><term>Récepteurs ErbB (métabolisme)</term><term>Souris</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère (métabolisme)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Transduction du signal</term><term>Virus du SRAS (pathogénicité)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Amphiregulin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amphiregulin</term><term>ErbB Receptors</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Amphiréguline</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Fibrose pulmonaire</term><term>Poumon</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Wound Healing</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Pulmonary Fibrosis</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Amphiréguline</term><term>Fibrose pulmonaire</term><term>Récepteurs ErbB</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Pulmonary Fibrosis</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Fibrose pulmonaire</term><term>Poumon</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term><term>Pulmonary Fibrosis</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cicatrisation de plaie</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic respiratory virus that causes morbidity and mortality in humans. After infection with SARS-CoV, the acute lung injury caused by the virus must be repaired to regain lung function. A dysregulation in this wound healing process leads to fibrosis. Many survivors of SARS-CoV infection develop pulmonary fibrosis (PF), with higher prevalence in older patients. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth factor receptor (EGFR), is critical to recovery from SARS-CoV-induced tissue damage. In mice with constitutively active EGFR [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection, the EGFR ligands amphiregulin and heparin-binding EGF-like growth factor (HB-EGF) are upregulated, and exogenous addition of these ligands during infection leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses.<b>IMPORTANCE</b> PF has many causative triggers, including severe respiratory viruses such as SARS-CoV. Currently there are no treatments to prevent the onset or limit the progression of PF, and the molecular pathways underlying the development of PF are not well understood. In this study, we identified a role for the balanced control of EGFR signaling as a key factor in progression to PF. These data demonstrate that therapeutic treatment modulating EGFR activation could protect against PF development caused by severe respiratory virus infection.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Venkataraman, Thiagarajan" sort="Venkataraman, Thiagarajan" uniqKey="Venkataraman T" first="Thiagarajan" last="Venkataraman">Thiagarajan Venkataraman</name></region><name sortKey="Coleman, Christopher M" sort="Coleman, Christopher M" uniqKey="Coleman C" first="Christopher M" last="Coleman">Christopher M. Coleman</name><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B" last="Frieman">Matthew B. Frieman</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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