MersV1, PubMed, Curation, bibRecord, 000918

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 : 000919

Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.

Source :

Emerging microbes & infections [ 2222-1751 ] ; 2018.

RBID : pubmed:29691378

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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<author><name sortKey="Guo, Renfeng" sort="Guo, Renfeng" uniqKey="Guo R" first="Renfeng" last="Guo">Renfeng Guo</name>
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<author><name sortKey="Sun, Shihui" sort="Sun, Shihui" uniqKey="Sun S" first="Shihui" last="Sun">Shihui Sun</name>
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<author><name sortKey="Zhou, Yusen" sort="Zhou, Yusen" uniqKey="Zhou Y" first="Yusen" last="Zhou">Yusen Zhou</name>
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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>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation du complément (immunologie)</term>
<term>Animaux</term>
<term>Apoptose</term>
<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>
<term>Humains</term>
<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>
<term>Interactions hôte-pathogène (immunologie)</term>
<term>Lymphocytes T (immunologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (immunologie)</term>
<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>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Complement Inactivating Agents</term>
</keywords>
<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>
</keywords>
<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>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term>
<term>Rate</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Complément C5a</term>
<term>Facteurs immunologiques</term>
<term>Récepteur à l'anaphylatoxine C5a</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Rate</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Spleen</term>
</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>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Complement Activation</term>
<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>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Apoptosis</term>
<term>Disease Models, Animal</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Humains</term>
<term>Infections à coronavirus</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
<term>Souris transgéniques</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>
</Pagination>
<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>
</Author>
<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>
</Author>
<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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<Author ValidYN="Y"><LastName>Guo</LastName>
<ForeName>Yan</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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<Author ValidYN="Y"><LastName>Li</LastName>
<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>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>04</Month>
<Day>24</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Emerg Microbes Infect</MedlineTA>
<NlmUniqueID>101594885</NlmUniqueID>
<ISSNLinking>2222-1751</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000591759">C5ar1 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018925">Chemokines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
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</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D044087">Receptor, Anaphylatoxin C5a</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>80295-54-1</RegistryNumber>
<NameOfSubstance UI="D015936">Complement C5a</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber>
<NameOfSubstance UI="C042807">DPP4 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber>
<NameOfSubstance UI="D018819">Dipeptidyl Peptidase 4</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018925" MajorTopicYN="N">Chemokines</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
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<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015936" MajorTopicYN="N">Complement C5a</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051056" MajorTopicYN="N">Complement Inactivating Agents</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D018819" MajorTopicYN="N">Dipeptidyl Peptidase 4</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
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<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName>
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<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
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<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
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<MeshHeading><DescriptorName UI="D013154" MajorTopicYN="N">Spleen</DescriptorName>
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<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
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HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 000918 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    MersV1
   |flux=    PubMed
   |étape=   Curation
   |type=    RBID
   |clé=     pubmed:29691378
   |texte=   Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i   -Sk "pubmed:29691378" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd   \
       | NlmPubMed2Wicri -a MersV1

This area was generated with Dilib version V0.6.33.
Data generation: Mon Apr 20 23:26:43 2020. Site generation: Sat Mar 27 09:06:09 2021

	Serveur d'exploration MERS
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration MERS

Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.

Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV.

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Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki