Middle East Respiratory Syndrome-Coronavirus Infection into Established hDPP4-Transgenic Mice Accelerates Lung Damage Via Activation of the Pro-Inflammatory Response and Pulmonary Fibrosis.
Identifieur interne : 002434 ( Ncbi/Merge ); précédent : 002433; suivant : 002435Middle East Respiratory Syndrome-Coronavirus Infection into Established hDPP4-Transgenic Mice Accelerates Lung Damage Via Activation of the Pro-Inflammatory Response and Pulmonary Fibrosis.
Auteurs : Ju Kim [Corée du Sud] ; Ye Lin Yang ; Yongsu Jeong [Corée du Sud] ; Yong-Suk Jang [Corée du Sud]Source :
- Journal of microbiology and biotechnology [ 1738-8872 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux, Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Dipeptidyl peptidase 4 (génétique), Dipeptidyl peptidase 4 (immunologie), Femelle, Fibrose pulmonaire (anatomopathologie), Fibrose pulmonaire (étiologie), Humains, Infections à coronavirus (), Infections à coronavirus (immunologie), Modèles animaux de maladie humaine, Poumon (anatomopathologie), Souris, Souris transgéniques.
- MESH :
- anatomopathologie : Fibrose pulmonaire, Poumon.
- génétique : Dipeptidyl peptidase 4.
- immunologie : Coronavirus du syndrome respiratoire du Moyen-Orient, Dipeptidyl peptidase 4, Infections à coronavirus.
- étiologie : Fibrose pulmonaire.
- Animaux, Femelle, Humains, Infections à coronavirus, Modèles animaux de maladie humaine, Souris, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Coronavirus Infections (complications), Coronavirus Infections (immunology), Dipeptidyl Peptidase 4 (genetics), Dipeptidyl Peptidase 4 (immunology), Disease Models, Animal, Female, Humans, Lung (pathology), Mice, Mice, Transgenic, Middle East Respiratory Syndrome Coronavirus (immunology), Pulmonary Fibrosis (etiology), Pulmonary Fibrosis (pathology).
- MESH :
- chemical , genetics : Dipeptidyl Peptidase 4.
- complications : Coronavirus Infections.
- etiology : Pulmonary Fibrosis.
- immunology : Coronavirus Infections, Dipeptidyl Peptidase 4, Middle East Respiratory Syndrome Coronavirus.
- pathology : Lung, Pulmonary Fibrosis.
- Animals, Disease Models, Animal, Female, Humans, Mice, Mice, Transgenic.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) infects the lower respiratory airway of humans, leading to severe acute respiratory failure. Unlike human dipeptidyl peptidase 4 (hDPP4), a receptor for MERS-CoV, mouse DPP4 (mDPP4) failed to support MERS-CoV infection. Consequently, diverse transgenic mouse models expressing hDPP4 have been developed using diverse methods, although some models show no mortality and/or only transient and mild-to-moderate clinical signs following MERS-CoV infection. Additionally, overexpressed hDPP4 is associated with neurological complications and breeding difficulties in some transgenic mice, resulting in impeding further studies. Here, we generated stable hDPP4-transgenic mice that were sufficiently susceptible to MERS-CoV infection. The transgenic mice showed weight loss, decreased pulmonary function, and increased mortality with minimal perturbation of overexpressed hDPP4 after MERS-CoV infection. In addition, we observed histopathological signs indicative of progressive pulmonary fibrosis, including thickened alveolar septa, infiltration of inflammatory monocytes, and macrophage polarization as well as elevated expression of profibrotic molecules and acute inflammatory response in the lung of MERS-CoV-infected hDPP4-transgenic mice. Collectively, we suggest that this hDPP4-transgenic mouse is useful in understanding the pathogenesis of MERS-CoV infection and for antiviral research and vaccine development against the virus.
DOI: 10.4014/jmb.1910.10055
PubMed: 31838832
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sortKey="Yang, Ye Lin" sort="Yang, Ye Lin" uniqKey="Yang Y" first="Ye Lin" last="Yang">Ye Lin Yang</name><affiliation><nlm:affiliation>Department of Bioactive Material Sciences and Research Center of Bioactive Materials, Jeonbuk National University, Jeonju 54896, Repubic of Korea.</nlm:affiliation><wicri:noCountry code="subField">Repubic of Korea</wicri:noCountry></affiliation></author><author><name sortKey="Jeong, Yongsu" sort="Jeong, Yongsu" uniqKey="Jeong Y" first="Yongsu" last="Jeong">Yongsu Jeong</name><affiliation wicri:level="1"><nlm:affiliation>Graduate School of Biotechnology, Kyung Hee University, Yongin 17104, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Graduate School of Biotechnology, Kyung Hee University, Yongin 17104</wicri:regionArea><wicri:noRegion>Yongin 17104</wicri:noRegion></affiliation></author><author><name sortKey="Jang, Yong Suk" sort="Jang, Yong Suk" uniqKey="Jang Y" first="Yong-Suk" last="Jang">Yong-Suk Jang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896</wicri:regionArea><wicri:noRegion>Jeonju 54896</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of microbiology and biotechnology</title><idno type="eISSN">1738-8872</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Coronavirus Infections (complications)</term><term>Coronavirus Infections (immunology)</term><term>Dipeptidyl Peptidase 4 (genetics)</term><term>Dipeptidyl Peptidase 4 (immunology)</term><term>Disease Models, Animal</term><term>Female</term><term>Humans</term><term>Lung (pathology)</term><term>Mice</term><term>Mice, Transgenic</term><term>Middle East Respiratory Syndrome Coronavirus (immunology)</term><term>Pulmonary Fibrosis (etiology)</term><term>Pulmonary Fibrosis (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie)</term><term>Dipeptidyl peptidase 4 (génétique)</term><term>Dipeptidyl peptidase 4 (immunologie)</term><term>Femelle</term><term>Fibrose pulmonaire (anatomopathologie)</term><term>Fibrose pulmonaire (étiologie)</term><term>Humains</term><term>Infections à coronavirus ()</term><term>Infections à coronavirus (immunologie)</term><term>Modèles animaux de maladie humaine</term><term>Poumon (anatomopathologie)</term><term>Souris</term><term>Souris transgéniques</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Dipeptidyl Peptidase 4</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Fibrose pulmonaire</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Coronavirus Infections</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Pulmonary Fibrosis</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>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Dipeptidyl peptidase 4</term><term>Infections à coronavirus</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus Infections</term><term>Dipeptidyl Peptidase 4</term><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Pulmonary Fibrosis</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Fibrose pulmonaire</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Humains</term><term>Infections à coronavirus</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Middle East respiratory syndrome coronavirus (MERS-CoV) infects the lower respiratory airway of humans, leading to severe acute respiratory failure. Unlike human dipeptidyl peptidase 4 (hDPP4), a receptor for MERS-CoV, mouse DPP4 (mDPP4) failed to support MERS-CoV infection. Consequently, diverse transgenic mouse models expressing hDPP4 have been developed using diverse methods, although some models show no mortality and/or only transient and mild-to-moderate clinical signs following MERS-CoV infection. Additionally, overexpressed hDPP4 is associated with neurological complications and breeding difficulties in some transgenic mice, resulting in impeding further studies. Here, we generated stable hDPP4-transgenic mice that were sufficiently susceptible to MERS-CoV infection. The transgenic mice showed weight loss, decreased pulmonary function, and increased mortality with minimal perturbation of overexpressed hDPP4 after MERS-CoV infection. In addition, we observed histopathological signs indicative of progressive pulmonary fibrosis, including thickened alveolar septa, infiltration of inflammatory monocytes, and macrophage polarization as well as elevated expression of profibrotic molecules and acute inflammatory response in the lung of MERS-CoV-infected hDPP4-transgenic mice. Collectively, we suggest that this hDPP4-transgenic mouse is useful in understanding the pathogenesis of MERS-CoV infection and for antiviral research and vaccine development against the virus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31838832</PMID><DateCompleted><Year>2020</Year><Month>04</Month><Day>10</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>10</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1738-8872</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>3</Issue><PubDate><Year>2020</Year><Month>Mar</Month><Day>28</Day></PubDate></JournalIssue><Title>Journal of microbiology and biotechnology</Title><ISOAbbreviation>J. Microbiol. Biotechnol.</ISOAbbreviation></Journal><ArticleTitle>Middle East Respiratory Syndrome-Coronavirus Infection into Established hDPP4-Transgenic Mice Accelerates Lung Damage Via Activation of the Pro-Inflammatory Response and Pulmonary Fibrosis.</ArticleTitle><Pagination><MedlinePgn>427-438</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4014/jmb.1910.10055</ELocationID><Abstract><AbstractText>Middle East respiratory syndrome coronavirus (MERS-CoV) infects the lower respiratory airway of humans, leading to severe acute respiratory failure. Unlike human dipeptidyl peptidase 4 (hDPP4), a receptor for MERS-CoV, mouse DPP4 (mDPP4) failed to support MERS-CoV infection. Consequently, diverse transgenic mouse models expressing hDPP4 have been developed using diverse methods, although some models show no mortality and/or only transient and mild-to-moderate clinical signs following MERS-CoV infection. Additionally, overexpressed hDPP4 is associated with neurological complications and breeding difficulties in some transgenic mice, resulting in impeding further studies. Here, we generated stable hDPP4-transgenic mice that were sufficiently susceptible to MERS-CoV infection. The transgenic mice showed weight loss, decreased pulmonary function, and increased mortality with minimal perturbation of overexpressed hDPP4 after MERS-CoV infection. In addition, we observed histopathological signs indicative of progressive pulmonary fibrosis, including thickened alveolar septa, infiltration of inflammatory monocytes, and macrophage polarization as well as elevated expression of profibrotic molecules and acute inflammatory response in the lung of MERS-CoV-infected hDPP4-transgenic mice. 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