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 : 000330 ( PubMed/Corpus ); précédent : 000329; suivant : 000331Middle 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 ; Ye Lin Yang ; Yongsu Jeong ; Yong-Suk JangSource :
- Journal of microbiology and biotechnology [ 1738-8872 ] ; 2020.
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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pubmed:31838832Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Middle East Respiratory Syndrome-Coronavirus Infection into Established hDPP4-Transgenic Mice Accelerates Lung Damage Via Activation of the Pro-Inflammatory Response and Pulmonary Fibrosis.</title><author><name sortKey="Kim, Ju" sort="Kim, Ju" uniqKey="Kim J" first="Ju" last="Kim">Ju Kim</name><affiliation><nlm:affiliation>Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896, Republic of Korea.</nlm:affiliation></affiliation></author><author><name 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></affiliation></author><author><name sortKey="Jeong, Yongsu" sort="Jeong, Yongsu" uniqKey="Jeong Y" first="Yongsu" last="Jeong">Yongsu Jeong</name><affiliation><nlm:affiliation>Graduate School of Biotechnology, Kyung Hee University, Yongin 17104, Republic of Korea.</nlm:affiliation></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><nlm:affiliation>Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896, Republic of Korea.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:31838832</idno><idno type="pmid">31838832</idno><idno type="doi">10.4014/jmb.1910.10055</idno><idno type="wicri:Area/PubMed/Corpus">000330</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000330</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Middle East Respiratory Syndrome-Coronavirus Infection into Established hDPP4-Transgenic Mice Accelerates Lung Damage Via Activation of the Pro-Inflammatory Response and Pulmonary Fibrosis.</title><author><name sortKey="Kim, Ju" sort="Kim, Ju" uniqKey="Kim J" first="Ju" last="Kim">Ju Kim</name><affiliation><nlm:affiliation>Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896, Republic of Korea.</nlm:affiliation></affiliation></author><author><name 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></affiliation></author><author><name sortKey="Jeong, Yongsu" sort="Jeong, Yongsu" uniqKey="Jeong Y" first="Yongsu" last="Jeong">Yongsu Jeong</name><affiliation><nlm:affiliation>Graduate School of Biotechnology, Kyung Hee University, Yongin 17104, Republic of Korea.</nlm:affiliation></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><nlm:affiliation>Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896, Republic of Korea.</nlm:affiliation></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="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Dipeptidyl Peptidase 4</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="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" 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></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. 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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Ju</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Molecular Biology and the Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ye Lin</ForeName><Initials>YL</Initials><AffiliationInfo><Affiliation>Department of Bioactive Material Sciences and Research Center of Bioactive Materials, Jeonbuk National University, Jeonju 54896, Repubic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jeong</LastName><ForeName>Yongsu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Graduate 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