Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice
Identifieur interne : 001037 ( Main/Exploration ); précédent : 001036; suivant : 001038Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice
Auteurs : Rudragouda Channappanavar [États-Unis] ; Anthony R. Fehr [États-Unis] ; Rahul Vijay [États-Unis] ; Matthias Mack [Allemagne] ; Jincun Zhao [États-Unis, République populaire de Chine] ; David K. Meyerholz [États-Unis] ; Stanley Perlman [États-Unis]Source :
- Cell Host & Microbe [ 1931-3128 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Femelle, Humains, Interféron de type I (génétique), Interféron de type I (immunologie), Macrophages (immunologie), Monocytes (immunologie), Pneumopathie infectieuse (génétique), Pneumopathie infectieuse (immunologie), Pneumopathie infectieuse (mortalité), Pneumopathie infectieuse (étiologie), Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (génétique), Virus du SRAS (immunologie), Virus du SRAS (physiologie).
- MESH :
- génétique : Interféron de type I, Pneumopathie infectieuse, Syndrome respiratoire aigu sévère, Virus du SRAS.
- immunologie : Interféron de type I, Macrophages, Monocytes, Pneumopathie infectieuse, Syndrome respiratoire aigu sévère, Virus du SRAS.
- mortalité : Pneumopathie infectieuse.
- physiologie : Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- étiologie : Pneumopathie infectieuse.
- Animaux, Femelle, Humains, Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère.
English descriptors
- KwdEn :
- Animals, Female, Humans, Interferon Type I (genetics), Interferon Type I (immunology), Macrophages (immunology), Mice, Mice, Inbred BALB C, Monocytes (immunology), Pneumonia (etiology), Pneumonia (genetics), Pneumonia (immunology), Pneumonia (mortality), SARS Virus (genetics), SARS Virus (immunology), SARS Virus (physiology), Severe Acute Respiratory Syndrome (complications), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , genetics : Interferon Type I.
- chemical , immunology : Interferon Type I.
- complications : Severe Acute Respiratory Syndrome.
- etiology : Pneumonia.
- genetics : Pneumonia, SARS Virus, Severe Acute Respiratory Syndrome.
- immunology : Macrophages, Monocytes, Pneumonia, SARS Virus, Severe Acute Respiratory Syndrome.
- mortality : Pneumonia.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Female, Humans, Mice, Mice, Inbred BALB C.
Abstract
Highly pathogenic human respiratory coronaviruses cause acute lethal disease characterized by exuberant inflammatory responses and lung damage. However, the factors leading to lung pathology are not well understood. Using mice infected with SARS (severe acute respiratory syndrome)-CoV, we show that robust virus replication accompanied by delayed type I interferon (IFN-I) signaling orchestrates inflammatory responses and lung immunopathology with diminished survival. IFN-I remains detectable until after virus titers peak, but early IFN-I administration ameliorates immunopathology. This delayed IFN-I signaling promotes the accumulation of pathogenic inflammatory monocyte-macrophages (IMMs), resulting in elevated lung cytokine/chemokine levels, vascular leakage, and impaired virus-specific T cell responses. Genetic ablation of the IFN-αβ receptor (IFNAR) or IMM depletion protects mice from lethal infection, without affecting viral load. These results demonstrate that IFN-I and IMM promote lethal SARS-CoV infection and identify IFN-I and IMMs as potential therapeutic targets in patients infected with pathogenic coronavirus and perhaps other respiratory viruses.
Url:
DOI: 10.1016/j.chom.2016.01.007
PubMed: 26867177
PubMed Central: 4752723
Affiliations:
- Allemagne, République populaire de Chine, États-Unis
- Guangdong, Iowa
- Iowa City, Jiangmen
- Université de l'Iowa
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Le document en format XML
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Fehr</name><affiliation wicri:level="4"><nlm:aff id="aff1">Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Iowa, Iowa City, IA 52242</wicri:regionArea><placeName><region type="state">Iowa</region><settlement type="city">Iowa City</settlement></placeName><orgName type="university">Université de l'Iowa</orgName></affiliation></author><author><name sortKey="Vijay, Rahul" sort="Vijay, Rahul" uniqKey="Vijay R" first="Rahul" last="Vijay">Rahul Vijay</name><affiliation wicri:level="4"><nlm:aff id="aff2">Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242</wicri:regionArea><placeName><region type="state">Iowa</region><settlement type="city">Iowa City</settlement></placeName><orgName type="university">Université de l'Iowa</orgName></affiliation></author><author><name sortKey="Mack, Matthias" sort="Mack, Matthias" uniqKey="Mack M" first="Matthias" last="Mack">Matthias Mack</name><affiliation wicri:level="1"><nlm:aff id="aff3">Department of Internal Medicine, University Hospital Regensburg, Regensburg 93042, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Internal Medicine, University Hospital Regensburg, Regensburg 93042</wicri:regionArea><wicri:noRegion>93042</wicri:noRegion><wicri:noRegion>93042</wicri:noRegion><wicri:noRegion>Regensburg 93042</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Jincun" sort="Zhao, Jincun" uniqKey="Zhao J" first="Jincun" last="Zhao">Jincun Zhao</name><affiliation wicri:level="4"><nlm:aff id="aff1">Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Iowa, Iowa City, IA 52242</wicri:regionArea><placeName><region type="state">Iowa</region><settlement type="city">Iowa City</settlement></placeName><orgName type="university">Université de l'Iowa</orgName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff4">State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120</wicri:regionArea><placeName><settlement type="city">Jiangmen</settlement><region type="province">Guangdong</region></placeName></affiliation></author><author><name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K." last="Meyerholz">David K. Meyerholz</name><affiliation wicri:level="4"><nlm:aff id="aff5">Department of Pathology, University of Iowa, Iowa City, IA 52242, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, University of Iowa, Iowa City, IA 52242</wicri:regionArea><placeName><region type="state">Iowa</region><settlement type="city">Iowa City</settlement></placeName><orgName type="university">Université de l'Iowa</orgName></affiliation></author><author><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><affiliation wicri:level="4"><nlm:aff id="aff1">Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, University of Iowa, Iowa City, IA 52242</wicri:regionArea><placeName><region type="state">Iowa</region><settlement type="city">Iowa City</settlement></placeName><orgName type="university">Université de l'Iowa</orgName></affiliation><affiliation wicri:level="4"><nlm:aff id="aff2">Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242</wicri:regionArea><placeName><region type="state">Iowa</region><settlement type="city">Iowa City</settlement></placeName><orgName type="university">Université de l'Iowa</orgName></affiliation></author></analytic><series><title level="j">Cell Host & Microbe</title><idno type="ISSN">1931-3128</idno><idno type="eISSN">1934-6069</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Female</term><term>Humans</term><term>Interferon Type I (genetics)</term><term>Interferon Type I (immunology)</term><term>Macrophages (immunology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Monocytes (immunology)</term><term>Pneumonia (etiology)</term><term>Pneumonia (genetics)</term><term>Pneumonia (immunology)</term><term>Pneumonia (mortality)</term><term>SARS Virus (genetics)</term><term>SARS Virus (immunology)</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (complications)</term><term>Severe Acute Respiratory Syndrome (genetics)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (virology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Humains</term><term>Interféron de type I (génétique)</term><term>Interféron de type I (immunologie)</term><term>Macrophages (immunologie)</term><term>Monocytes (immunologie)</term><term>Pneumopathie infectieuse (génétique)</term><term>Pneumopathie infectieuse (immunologie)</term><term>Pneumopathie infectieuse (mortalité)</term><term>Pneumopathie infectieuse (étiologie)</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Syndrome respiratoire aigu sévère ()</term><term>Syndrome respiratoire aigu sévère (génétique)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Pneumonia</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interféron de type I</term><term>Pneumopathie infectieuse</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interféron de type I</term><term>Macrophages</term><term>Monocytes</term><term>Pneumopathie infectieuse</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Macrophages</term><term>Monocytes</term><term>Pneumonia</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="mortalité" xml:lang="fr"><term>Pneumopathie infectieuse</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>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Humans</term><term>Mice</term><term>Mice, Inbred BALB C</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Humains</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Summary</title><p>Highly pathogenic human respiratory coronaviruses cause acute lethal disease characterized by exuberant inflammatory responses and lung damage. However, the factors leading to lung pathology are not well understood. Using mice infected with SARS (severe acute respiratory syndrome)-CoV, we show that robust virus replication accompanied by delayed type I interferon (IFN-I) signaling orchestrates inflammatory responses and lung immunopathology with diminished survival. IFN-I remains detectable until after virus titers peak, but early IFN-I administration ameliorates immunopathology. This delayed IFN-I signaling promotes the accumulation of pathogenic inflammatory monocyte-macrophages (IMMs), resulting in elevated lung cytokine/chemokine levels, vascular leakage, and impaired virus-specific T cell responses. Genetic ablation of the IFN-αβ receptor (IFNAR) or IMM depletion protects mice from lethal infection, without affecting viral load. These results demonstrate that IFN-I and IMM promote lethal SARS-CoV infection and identify IFN-I and IMMs as potential therapeutic targets in patients infected with pathogenic coronavirus and perhaps other respiratory viruses.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Aldridge, J R" uniqKey="Aldridge J">J.R. Aldridge</name></author><author><name sortKey="Moseley, C E" uniqKey="Moseley C">C.E. Moseley</name></author><author><name sortKey="Boltz, D A" uniqKey="Boltz D">D.A. Boltz</name></author><author><name sortKey="Negovetich, N J" uniqKey="Negovetich N">N.J. Negovetich</name></author><author><name sortKey="Reynolds, C" uniqKey="Reynolds C">C. Reynolds</name></author><author><name sortKey="Franks, J" uniqKey="Franks J">J. Franks</name></author><author><name sortKey="Brown, S A" uniqKey="Brown S">S.A. Brown</name></author><author><name sortKey="Doherty, P C" uniqKey="Doherty P">P.C. 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Meyerholz</name><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><name sortKey="Vijay, Rahul" sort="Vijay, Rahul" uniqKey="Vijay R" first="Rahul" last="Vijay">Rahul Vijay</name><name sortKey="Zhao, Jincun" sort="Zhao, Jincun" uniqKey="Zhao J" first="Jincun" last="Zhao">Jincun Zhao</name></country><country name="Allemagne"><noRegion><name sortKey="Mack, Matthias" sort="Mack, Matthias" uniqKey="Mack M" first="Matthias" last="Mack">Matthias Mack</name></noRegion></country><country name="République populaire de Chine"><region name="Guangdong"><name sortKey="Zhao, Jincun" sort="Zhao, Jincun" uniqKey="Zhao J" first="Jincun" last="Zhao">Jincun Zhao</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice
}}
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:26867177" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a SrasV1
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