Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis
Identifieur interne : 000D04 ( Main/Exploration ); précédent : 000D03; suivant : 000D05Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis
Auteurs : Lisa E. Gralinski [États-Unis] ; Timothy P. Sheahan [États-Unis] ; Thomas E. Morrison [États-Unis] ; Vineet D. Menachery [États-Unis] ; Kara Jensen [États-Unis] ; Sarah R. Leist [États-Unis] ; Alan Whitmore [États-Unis] ; Mark T. Heise [États-Unis] ; Ralph S. Baric [États-Unis]Source :
- mBio [ 2150-7511 ] ; 2018.
Descripteurs français
- KwdFr :
- Activation du complément, Animaux, Charge virale, Chimiokines (sang), Complément C3 (déficit), Complément C3 (génétique), Cytokines (sang), Femelle, Immunité innée, Interactions hôte-pathogène (immunologie), Modèles animaux de maladie humaine, Poumon (anatomopathologie), Poumon (immunologie), Poumon (virologie), Réplication virale, Souris, Souris de lignée C57BL, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Poumon.
- déficit : Complément C3.
- génétique : Complément C3.
- immunologie : Interactions hôte-pathogène, Poumon, Syndrome respiratoire aigu sévère, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- sang : Chimiokines, Cytokines.
- virologie : Poumon, Syndrome respiratoire aigu sévère.
- Activation du complément, Animaux, Charge virale, Femelle, Immunité innée, Modèles animaux de maladie humaine, Réplication virale, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals, Chemokines (blood), Complement Activation, Complement C3 (deficiency), Complement C3 (genetics), Cytokines (blood), Disease Models, Animal, Female, Host-Pathogen Interactions (immunology), Immunity, Innate, Lung (immunology), Lung (pathology), Lung (virology), Mice, Mice, Inbred C57BL, SARS Virus (immunology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Viral Load, Virus Replication.
- MESH :
- chemical , blood : Chemokines, Cytokines.
- chemical , deficiency : Complement C3.
- chemical , genetics : Complement C3.
- immunology : Host-Pathogen Interactions, Lung, SARS Virus, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Lung.
- virology : Lung, Severe Acute Respiratory Syndrome.
- Animals, Complement Activation, Disease Models, Animal, Female, Immunity, Innate, Mice, Mice, Inbred C57BL, Viral Load, Virus Replication.
Abstract
The complement system is a critical part of host defense to many bacterial, viral, and fungal infections. It works alongside pattern recognition receptors to stimulate host defense systems in advance of activation of the adaptive immune response. In this study, we directly test the role of complement in SARS-CoV pathogenesis using a mouse model and show that respiratory disease is significantly reduced in the absence of complement even though viral load is unchanged. Complement-deficient mice have reduced neutrophilia in their lungs and reduced systemic inflammation, consistent with the observation that SARS-CoV pathogenesis is an immune-driven disease. These data suggest that inhibition of complement signaling might be an effective treatment option following coronavirus infection.
Url:
DOI: 10.1128/mBio.01753-18
PubMed: 30301856
PubMed Central: 6178621
Affiliations:
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Le document en format XML
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Heise</name><affiliation wicri:level="2"><nlm:aff id="aff4"><addr-line>Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, USA</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Genetics, University of North Carolina, Chapel Hill, North Carolina</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author><author><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S." last="Baric">Ralph S. Baric</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author></analytic><series><title level="j">mBio</title><idno type="eISSN">2150-7511</idno><imprint><date when="2018">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Chemokines (blood)</term><term>Complement Activation</term><term>Complement C3 (deficiency)</term><term>Complement C3 (genetics)</term><term>Cytokines (blood)</term><term>Disease Models, Animal</term><term>Female</term><term>Host-Pathogen Interactions (immunology)</term><term>Immunity, Innate</term><term>Lung (immunology)</term><term>Lung (pathology)</term><term>Lung (virology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Viral Load</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation du complément</term><term>Animaux</term><term>Charge virale</term><term>Chimiokines (sang)</term><term>Complément C3 (déficit)</term><term>Complément C3 (génétique)</term><term>Cytokines (sang)</term><term>Femelle</term><term>Immunité innée</term><term>Interactions hôte-pathogène (immunologie)</term><term>Modèles animaux de maladie humaine</term><term>Poumon (anatomopathologie)</term><term>Poumon (immunologie)</term><term>Poumon (virologie)</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Chemokines</term><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Complement C3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Complement C3</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Complément C3</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Complément C3</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interactions hôte-pathogène</term><term>Poumon</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Host-Pathogen Interactions</term><term>Lung</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</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></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Chimiokines</term><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Poumon</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Complement Activation</term><term>Disease Models, Animal</term><term>Female</term><term>Immunity, Innate</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Viral Load</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation du complément</term><term>Animaux</term><term>Charge virale</term><term>Femelle</term><term>Immunité innée</term><term>Modèles animaux de maladie humaine</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The complement system is a critical part of host defense to many bacterial, viral, and fungal infections. It works alongside pattern recognition receptors to stimulate host defense systems in advance of activation of the adaptive immune response. In this study, we directly test the role of complement in SARS-CoV pathogenesis using a mouse model and show that respiratory disease is significantly reduced in the absence of complement even though viral load is unchanged. Complement-deficient mice have reduced neutrophilia in their lungs and reduced systemic inflammation, consistent with the observation that SARS-CoV pathogenesis is an immune-driven disease. These data suggest that inhibition of complement signaling might be an effective treatment option following coronavirus infection.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Rota, Pa" uniqKey="Rota P">PA Rota</name></author><author><name sortKey="Oberste, Ms" uniqKey="Oberste M">MS Oberste</name></author><author><name sortKey="Monroe, Ss" uniqKey="Monroe S">SS Monroe</name></author><author><name sortKey="Nix, Wa" uniqKey="Nix W">WA Nix</name></author><author><name sortKey="Campagnoli, R" uniqKey="Campagnoli R">R Campagnoli</name></author><author><name sortKey="Icenogle, Jp" uniqKey="Icenogle J">JP Icenogle</name></author><author><name sortKey="Pe Aranda, S" uniqKey="Pe Aranda S">S Peñaranda</name></author><author><name sortKey="Bankamp, B" uniqKey="Bankamp B">B Bankamp</name></author><author><name sortKey="Maher, K" uniqKey="Maher K">K Maher</name></author><author><name sortKey="Chen, Mh" 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Denison</name></author><author><name sortKey="Geisbert, T" uniqKey="Geisbert T">T Geisbert</name></author><author><name sortKey="Baric, R" uniqKey="Baric R">R Baric</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sheahan, T" uniqKey="Sheahan T">T Sheahan</name></author><author><name sortKey="Rockx, B" uniqKey="Rockx B">B Rockx</name></author><author><name sortKey="Donaldson, E" uniqKey="Donaldson E">E Donaldson</name></author><author><name sortKey="Sims, A" uniqKey="Sims A">A Sims</name></author><author><name sortKey="Pickles, R" uniqKey="Pickles R">R Pickles</name></author><author><name sortKey="Corti, D" uniqKey="Corti D">D Corti</name></author><author><name sortKey="Baric, R" uniqKey="Baric R">R Baric</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Misharin, Av" uniqKey="Misharin A">AV Misharin</name></author><author><name sortKey="Morales Nebreda, L" uniqKey="Morales Nebreda L">L Morales-Nebreda</name></author><author><name sortKey="Mutlu, Gm" uniqKey="Mutlu G">GM Mutlu</name></author><author><name sortKey="Budinger, Gr" uniqKey="Budinger G">GR Budinger</name></author><author><name sortKey="Perlman, H" uniqKey="Perlman H">H Perlman</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Caroline du Nord</li><li>Colorado</li><li>Texas</li></region></list><tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Gralinski, Lisa E" sort="Gralinski, Lisa E" uniqKey="Gralinski L" first="Lisa E." last="Gralinski">Lisa E. Gralinski</name></region><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S." last="Baric">Ralph S. Baric</name><name sortKey="Heise, Mark T" sort="Heise, Mark T" uniqKey="Heise M" first="Mark T." last="Heise">Mark T. Heise</name><name sortKey="Jensen, Kara" sort="Jensen, Kara" uniqKey="Jensen K" first="Kara" last="Jensen">Kara Jensen</name><name sortKey="Leist, Sarah R" sort="Leist, Sarah R" uniqKey="Leist S" first="Sarah R." last="Leist">Sarah R. Leist</name><name sortKey="Menachery, Vineet D" sort="Menachery, Vineet D" uniqKey="Menachery V" first="Vineet D." last="Menachery">Vineet D. Menachery</name><name sortKey="Menachery, Vineet D" sort="Menachery, Vineet D" uniqKey="Menachery V" first="Vineet D." last="Menachery">Vineet D. Menachery</name><name sortKey="Morrison, Thomas E" sort="Morrison, Thomas E" uniqKey="Morrison T" first="Thomas E." last="Morrison">Thomas E. Morrison</name><name sortKey="Sheahan, Timothy P" sort="Sheahan, Timothy P" uniqKey="Sheahan T" first="Timothy P." last="Sheahan">Timothy P. Sheahan</name><name sortKey="Whitmore, Alan" sort="Whitmore, Alan" uniqKey="Whitmore A" first="Alan" last="Whitmore">Alan Whitmore</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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