Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.
Identifieur interne : 000918 ( PubMed/Curation ); précédent : 000917; suivant : 000919Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.
Auteurs : Yuting Jiang [République populaire de Chine] ; Guangyu Zhao [République populaire de Chine] ; Nianping Song [République populaire de Chine] ; Pei Li [République populaire de Chine] ; Yuehong Chen [République populaire de Chine] ; Yan Guo [République populaire de Chine] ; Junfeng Li [République populaire de Chine] ; Lanying Du [États-Unis] ; Shibo Jiang [États-Unis] ; Renfeng Guo [Allemagne] ; Shihui Sun [République populaire de Chine] ; Yusen Zhou [République populaire de Chine]Source :
- Emerging microbes & infections [ 2222-1751 ] ; 2018.
Descripteurs français
- KwdFr :
- Activation du complément (immunologie), Animaux, Apoptose, Chimiokines (immunologie), Complément C5a (antagonistes et inhibiteurs), Complément C5a (immunologie), Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité), Cytokines (immunologie), Dipeptidyl peptidase 4 (génétique), Facteurs immunologiques (antagonistes et inhibiteurs), Facteurs immunologiques (immunologie), Humains, Infections à coronavirus (), Infections à coronavirus (immunologie), Infections à coronavirus (virologie), Inhibiteurs du complément (administration et posologie), Inhibiteurs du complément (immunologie), Interactions hôte-pathogène (immunologie), Lymphocytes T (immunologie), Modèles animaux de maladie humaine, Poumon (anatomopathologie), Poumon (immunologie), Poumon (virologie), Rate (anatomopathologie), Rate (cytologie), Rate (immunologie), Rate (virologie), Récepteur à l'anaphylatoxine C5a (antagonistes et inhibiteurs), Réplication virale (immunologie), Souris, Souris transgéniques.
- MESH :
- administration et posologie : Inhibiteurs du complément.
- anatomopathologie : Poumon, Rate.
- antagonistes et inhibiteurs : Complément C5a, Facteurs immunologiques, Récepteur à l'anaphylatoxine C5a.
- cytologie : Rate.
- génétique : Dipeptidyl peptidase 4.
- immunologie : Activation du complément, Chimiokines, Complément C5a, Coronavirus du syndrome respiratoire du Moyen-Orient, Cytokines, Facteurs immunologiques, Infections à coronavirus, Inhibiteurs du complément, Interactions hôte-pathogène, Lymphocytes T, Poumon, Rate, Réplication virale.
- pathogénicité : Coronavirus du syndrome respiratoire du Moyen-Orient.
- virologie : Infections à coronavirus, Poumon, Rate.
- Animaux, Apoptose, Humains, Infections à coronavirus, Modèles animaux de maladie humaine, Souris, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Apoptosis, Chemokines (immunology), Complement Activation (immunology), Complement C5a (antagonists & inhibitors), Complement C5a (immunology), Complement Inactivating Agents (administration & dosage), Complement Inactivating Agents (immunology), Coronavirus Infections (immunology), Coronavirus Infections (therapy), Coronavirus Infections (virology), Cytokines (immunology), Dipeptidyl Peptidase 4 (genetics), Disease Models, Animal, Host-Pathogen Interactions (immunology), Humans, Immunologic Factors (antagonists & inhibitors), Immunologic Factors (immunology), Lung (immunology), Lung (pathology), Lung (virology), Mice, Mice, Transgenic, Middle East Respiratory Syndrome Coronavirus (immunology), Middle East Respiratory Syndrome Coronavirus (pathogenicity), Receptor, Anaphylatoxin C5a (antagonists & inhibitors), Spleen (cytology), Spleen (immunology), Spleen (pathology), Spleen (virology), T-Lymphocytes (immunology), Virus Replication (immunology).
- MESH :
- chemical , administration & dosage : Complement Inactivating Agents.
- chemical , antagonists & inhibitors : Complement C5a, Immunologic Factors, Receptor, Anaphylatoxin C5a.
- chemical , genetics : Dipeptidyl Peptidase 4.
- chemical , immunology : Chemokines, Complement C5a, Complement Inactivating Agents, Cytokines, Immunologic Factors.
- cytology : Spleen.
- immunology : Complement Activation, Coronavirus Infections, Host-Pathogen Interactions, Lung, Middle East Respiratory Syndrome Coronavirus, Spleen, T-Lymphocytes, Virus Replication.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus.
- pathology : Lung, Spleen.
- therapy : Coronavirus Infections.
- virology : Coronavirus Infections, Lung, Spleen.
- Animals, Apoptosis, Disease Models, Animal, Humans, Mice, Mice, Transgenic.
Abstract
The pathogenesis of highly pathogenic Middle East respiratory syndrome coronavirus (MERS-CoV) remains poorly understood. In a previous study, we established an hDPP4-transgenic (hDPP4-Tg) mouse model in which MERS-CoV infection causes severe acute respiratory failure and high mortality accompanied by an elevated secretion of cytokines and chemokines. Since excessive complement activation is an important factor that contributes to acute lung injury after viral infection, in this study, we investigated the role of complement in MERS-CoV-induced lung damage. Our study showed that complement was excessively activated in MERS-CoV-infected hDPP4-Tg mice through observations of increased concentrations of the C5a and C5b-9 complement activation products in sera and lung tissues, respectively. Interestingly, blocking C5a production by targeting its receptor, C5aR, alleviated lung and spleen tissue damage and reduced inflammatory responses. More importantly, anti-C5aR antibody treatment led to decreased viral replication in lung tissues. Furthermore, compared with the sham treatment control, apoptosis of splenic cells was less pronounced in the splenic white pulp of treated mice, and greater number of proliferating splenic cells, particularly in the red pulp, was observed. These data indicate that (1) dysregulated host immune responses contribute to the severe outcome of MERS; (2) excessive complement activation, triggered by MERS-CoV infection, promote such dysregulation; and (3) blockade of the C5a-C5aR axis lead to the decreased tissue damage induced by MERS-CoV infection, as manifested by reduced apoptosis and T cell regeneration in the spleen. Therefore, the results of this study suggest a new strategy for clinical intervention and adjunctive treatment in MERS-CoV cases.
DOI: 10.1038/s41426-018-0063-8
PubMed: 29691378
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<term>Apoptosis</term>
<term>Chemokines (immunology)</term>
<term>Complement Activation (immunology)</term>
<term>Complement C5a (antagonists & inhibitors)</term>
<term>Complement C5a (immunology)</term>
<term>Complement Inactivating Agents (administration & dosage)</term>
<term>Complement Inactivating Agents (immunology)</term>
<term>Coronavirus Infections (immunology)</term>
<term>Coronavirus Infections (therapy)</term>
<term>Coronavirus Infections (virology)</term>
<term>Cytokines (immunology)</term>
<term>Dipeptidyl Peptidase 4 (genetics)</term>
<term>Disease Models, Animal</term>
<term>Host-Pathogen Interactions (immunology)</term>
<term>Humans</term>
<term>Immunologic Factors (antagonists & inhibitors)</term>
<term>Immunologic Factors (immunology)</term>
<term>Lung (immunology)</term>
<term>Lung (pathology)</term>
<term>Lung (virology)</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
<term>Middle East Respiratory Syndrome Coronavirus (immunology)</term>
<term>Middle East Respiratory Syndrome Coronavirus (pathogenicity)</term>
<term>Receptor, Anaphylatoxin C5a (antagonists & inhibitors)</term>
<term>Spleen (cytology)</term>
<term>Spleen (immunology)</term>
<term>Spleen (pathology)</term>
<term>Spleen (virology)</term>
<term>T-Lymphocytes (immunology)</term>
<term>Virus Replication (immunology)</term>
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<term>Chimiokines (immunologie)</term>
<term>Complément C5a (antagonistes et inhibiteurs)</term>
<term>Complément C5a (immunologie)</term>
<term>Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie)</term>
<term>Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité)</term>
<term>Cytokines (immunologie)</term>
<term>Dipeptidyl peptidase 4 (génétique)</term>
<term>Facteurs immunologiques (antagonistes et inhibiteurs)</term>
<term>Facteurs immunologiques (immunologie)</term>
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<term>Infections à coronavirus ()</term>
<term>Infections à coronavirus (immunologie)</term>
<term>Infections à coronavirus (virologie)</term>
<term>Inhibiteurs du complément (administration et posologie)</term>
<term>Inhibiteurs du complément (immunologie)</term>
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<term>Modèles animaux de maladie humaine</term>
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<term>Poumon (virologie)</term>
<term>Rate (anatomopathologie)</term>
<term>Rate (cytologie)</term>
<term>Rate (immunologie)</term>
<term>Rate (virologie)</term>
<term>Récepteur à l'anaphylatoxine C5a (antagonistes et inhibiteurs)</term>
<term>Réplication virale (immunologie)</term>
<term>Souris</term>
<term>Souris transgéniques</term>
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<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Complement C5a</term>
<term>Immunologic Factors</term>
<term>Receptor, Anaphylatoxin C5a</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Dipeptidyl Peptidase 4</term>
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<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Chemokines</term>
<term>Complement C5a</term>
<term>Complement Inactivating Agents</term>
<term>Cytokines</term>
<term>Immunologic Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Inhibiteurs du complément</term>
</keywords>
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<term>Rate</term>
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<term>Facteurs immunologiques</term>
<term>Récepteur à l'anaphylatoxine C5a</term>
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</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Dipeptidyl peptidase 4</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Activation du complément</term>
<term>Chimiokines</term>
<term>Complément C5a</term>
<term>Coronavirus du syndrome respiratoire du Moyen-Orient</term>
<term>Cytokines</term>
<term>Facteurs immunologiques</term>
<term>Infections à coronavirus</term>
<term>Inhibiteurs du complément</term>
<term>Interactions hôte-pathogène</term>
<term>Lymphocytes T</term>
<term>Poumon</term>
<term>Rate</term>
<term>Réplication virale</term>
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<term>Coronavirus Infections</term>
<term>Host-Pathogen Interactions</term>
<term>Lung</term>
<term>Middle East Respiratory Syndrome Coronavirus</term>
<term>Spleen</term>
<term>T-Lymphocytes</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
<term>Spleen</term>
</keywords>
<keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Coronavirus Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Poumon</term>
<term>Rate</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Lung</term>
<term>Spleen</term>
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<term>Apoptosis</term>
<term>Disease Models, Animal</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
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<term>Apoptose</term>
<term>Humains</term>
<term>Infections à coronavirus</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">The pathogenesis of highly pathogenic Middle East respiratory syndrome coronavirus (MERS-CoV) remains poorly understood. In a previous study, we established an hDPP4-transgenic (hDPP4-Tg) mouse model in which MERS-CoV infection causes severe acute respiratory failure and high mortality accompanied by an elevated secretion of cytokines and chemokines. Since excessive complement activation is an important factor that contributes to acute lung injury after viral infection, in this study, we investigated the role of complement in MERS-CoV-induced lung damage. Our study showed that complement was excessively activated in MERS-CoV-infected hDPP4-Tg mice through observations of increased concentrations of the C5a and C5b-9 complement activation products in sera and lung tissues, respectively. Interestingly, blocking C5a production by targeting its receptor, C5aR, alleviated lung and spleen tissue damage and reduced inflammatory responses. More importantly, anti-C5aR antibody treatment led to decreased viral replication in lung tissues. Furthermore, compared with the sham treatment control, apoptosis of splenic cells was less pronounced in the splenic white pulp of treated mice, and greater number of proliferating splenic cells, particularly in the red pulp, was observed. These data indicate that (1) dysregulated host immune responses contribute to the severe outcome of MERS; (2) excessive complement activation, triggered by MERS-CoV infection, promote such dysregulation; and (3) blockade of the C5a-C5aR axis lead to the decreased tissue damage induced by MERS-CoV infection, as manifested by reduced apoptosis and T cell regeneration in the spleen. Therefore, the results of this study suggest a new strategy for clinical intervention and adjunctive treatment in MERS-CoV cases.</div>
</front>
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<DateCompleted><Year>2018</Year>
<Month>11</Month>
<Day>15</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>15</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2222-1751</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>1</Issue>
<PubDate><Year>2018</Year>
<Month>Apr</Month>
<Day>24</Day>
</PubDate>
</JournalIssue>
<Title>Emerging microbes & infections</Title>
<ISOAbbreviation>Emerg Microbes Infect</ISOAbbreviation>
</Journal>
<ArticleTitle>Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.</ArticleTitle>
<Pagination><MedlinePgn>77</MedlinePgn>
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<ELocationID EIdType="doi" ValidYN="Y">10.1038/s41426-018-0063-8</ELocationID>
<Abstract><AbstractText>The pathogenesis of highly pathogenic Middle East respiratory syndrome coronavirus (MERS-CoV) remains poorly understood. In a previous study, we established an hDPP4-transgenic (hDPP4-Tg) mouse model in which MERS-CoV infection causes severe acute respiratory failure and high mortality accompanied by an elevated secretion of cytokines and chemokines. Since excessive complement activation is an important factor that contributes to acute lung injury after viral infection, in this study, we investigated the role of complement in MERS-CoV-induced lung damage. Our study showed that complement was excessively activated in MERS-CoV-infected hDPP4-Tg mice through observations of increased concentrations of the C5a and C5b-9 complement activation products in sera and lung tissues, respectively. Interestingly, blocking C5a production by targeting its receptor, C5aR, alleviated lung and spleen tissue damage and reduced inflammatory responses. More importantly, anti-C5aR antibody treatment led to decreased viral replication in lung tissues. Furthermore, compared with the sham treatment control, apoptosis of splenic cells was less pronounced in the splenic white pulp of treated mice, and greater number of proliferating splenic cells, particularly in the red pulp, was observed. These data indicate that (1) dysregulated host immune responses contribute to the severe outcome of MERS; (2) excessive complement activation, triggered by MERS-CoV infection, promote such dysregulation; and (3) blockade of the C5a-C5aR axis lead to the decreased tissue damage induced by MERS-CoV infection, as manifested by reduced apoptosis and T cell regeneration in the spleen. Therefore, the results of this study suggest a new strategy for clinical intervention and adjunctive treatment in MERS-CoV cases.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Yuting</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Guangyu</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Song</LastName>
<ForeName>Nianping</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Pei</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Yuehong</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Yan</ForeName>
<Initials>Y</Initials>
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</AffiliationInfo>
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<ForeName>Junfeng</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Du</LastName>
<ForeName>Lanying</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Lindsley F. Kimball Research Institute, New York Blood Center, New York, NY, 10065, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Shibo</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Lindsley F. Kimball Research Institute, New York Blood Center, New York, NY, 10065, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Shanghai Medical College, Fudan University, Shanghai, 200032, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Guo</LastName>
<ForeName>Renfeng</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>InflaRx GmbH, Jena, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Shihui</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China. sunsh01@163.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Yusen</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, 100071, China. yszhou@bmi.ac.cn.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
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</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>04</Month>
<Day>24</Day>
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<MedlineTA>Emerg Microbes Infect</MedlineTA>
<NlmUniqueID>101594885</NlmUniqueID>
<ISSNLinking>2222-1751</ISSNLinking>
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