ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia.
Identifieur interne : 001257 ( Ncbi/Merge ); précédent : 001256; suivant : 001258ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia.
Auteurs : Hong Peng Jia [États-Unis] ; Dwight C. Look ; Lei Shi ; Melissa Hickey ; Lecia Pewe ; Jason Netland ; Michael Farzan ; Christine Wohlford-Lenane ; Stanley Perlman ; Paul B. MccraySource :
- Journal of virology [ 0022-538X ] ; 2005.
Descripteurs français
- KwdFr :
- Carboxypeptidases (métabolisme), Cellules épithéliales (), Cellules épithéliales (cytologie), Cellules épithéliales (virologie), Différenciation cellulaire, Humains, Infections à coronavirus (enzymologie), Infections à coronavirus (métabolisme), Lignée cellulaire, Peptidyl-Dipeptidase A, Récepteurs viraux (métabolisme), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (physiopathologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (métabolisme).
- MESH :
- anatomopathologie : Syndrome respiratoire aigu sévère.
- cytologie : Cellules épithéliales.
- enzymologie : Infections à coronavirus.
- métabolisme : Carboxypeptidases, Infections à coronavirus, Récepteurs viraux, Virus du SRAS.
- physiopathologie : Syndrome respiratoire aigu sévère.
- virologie : Cellules épithéliales, Syndrome respiratoire aigu sévère.
- Cellules épithéliales, Différenciation cellulaire, Humains, Lignée cellulaire, Peptidyl-Dipeptidase A.
English descriptors
- KwdEn :
- Carboxypeptidases (metabolism), Cell Differentiation, Cell Line, Coronavirus Infections (enzymology), Coronavirus Infections (metabolism), Epithelial Cells (chemistry), Epithelial Cells (cytology), Epithelial Cells (virology), Humans, Peptidyl-Dipeptidase A, Receptors, Virus (metabolism), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (physiopathology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , metabolism : Carboxypeptidases, Receptors, Virus.
- chemistry : Epithelial Cells.
- cytology : Epithelial Cells.
- enzymology : Coronavirus Infections.
- metabolism : Coronavirus Infections, SARS Virus.
- pathology : Severe Acute Respiratory Syndrome.
- physiopathology : Severe Acute Respiratory Syndrome.
- virology : Epithelial Cells, Severe Acute Respiratory Syndrome.
- Cell Differentiation, Cell Line, Humans, Peptidyl-Dipeptidase A.
Abstract
Studies of patients with severe acute respiratory syndrome (SARS) demonstrate that the respiratory tract is a major site of SARS-coronavirus (CoV) infection and disease morbidity. We studied host-pathogen interactions using native lung tissue and a model of well-differentiated cultures of primary human airway epithelia. Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.
DOI: 10.1128/JVI.79.23.14614-14621.2005
PubMed: 16282461
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pubmed:16282461Le document en format XML
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We studied host-pathogen interactions using native lung tissue and a model of well-differentiated cultures of primary human airway epithelia. Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16282461</PMID><DateCompleted><Year>2006</Year><Month>01</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>79</Volume><Issue>23</Issue><PubDate><Year>2005</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia.</ArticleTitle><Pagination><MedlinePgn>14614-21</MedlinePgn></Pagination><Abstract><AbstractText>Studies of patients with severe acute respiratory syndrome (SARS) demonstrate that the respiratory tract is a major site of SARS-coronavirus (CoV) infection and disease morbidity. We studied host-pathogen interactions using native lung tissue and a model of well-differentiated cultures of primary human airway epithelia. Angiotensin converting enzyme 2 (ACE2), the receptor for both the SARS-CoV and the related human respiratory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma. As assessed by immunofluorescence staining and membrane biotinylation, ACE2 protein was more abundantly expressed on the apical than the basolateral surface of polarized airway epithelia. Interestingly, ACE2 expression positively correlated with the differentiation state of epithelia. Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jia</LastName><ForeName>Hong Peng</ForeName><Initials>HP</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, 240-G EMRB, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Look</LastName><ForeName>Dwight C</ForeName><Initials>DC</Initials></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Lei</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Hickey</LastName><ForeName>Melissa</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Pewe</LastName><ForeName>Lecia</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Netland</LastName><ForeName>Jason</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Farzan</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Wohlford-Lenane</LastName><ForeName>Christine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Perlman</LastName><ForeName>Stanley</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>McCray</LastName><ForeName>Paul B</ForeName><Initials>PB</Initials><Suffix>Jr</Suffix></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 AI060699</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 DK054759</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AI060699-01</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 DK-54759</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.-</RegistryNumber><NameOfSubstance UI="D002268">Carboxypeptidases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.15.1</RegistryNumber><NameOfSubstance UI="D007703">Peptidyl-Dipeptidase A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.17.-</RegistryNumber><NameOfSubstance UI="C413524">angiotensin converting enzyme 2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002268" MajorTopicYN="N">Carboxypeptidases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011991" MajorTopicYN="N">Receptors, Virus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000821" 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uniqKey="Farzan M" first="Michael" last="Farzan">Michael Farzan</name><name sortKey="Hickey, Melissa" sort="Hickey, Melissa" uniqKey="Hickey M" first="Melissa" last="Hickey">Melissa Hickey</name><name sortKey="Look, Dwight C" sort="Look, Dwight C" uniqKey="Look D" first="Dwight C" last="Look">Dwight C. Look</name><name sortKey="Mccray, Paul B" sort="Mccray, Paul B" uniqKey="Mccray P" first="Paul B" last="Mccray">Paul B. Mccray</name><name sortKey="Netland, Jason" sort="Netland, Jason" uniqKey="Netland J" first="Jason" last="Netland">Jason Netland</name><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><name sortKey="Pewe, Lecia" sort="Pewe, Lecia" uniqKey="Pewe L" first="Lecia" last="Pewe">Lecia Pewe</name><name sortKey="Shi, Lei" sort="Shi, Lei" uniqKey="Shi L" first="Lei" last="Shi">Lei Shi</name><name sortKey="Wohlford Lenane, Christine" sort="Wohlford Lenane, Christine" uniqKey="Wohlford Lenane C" first="Christine" last="Wohlford-Lenane">Christine Wohlford-Lenane</name></noCountry><country name="États-Unis"><region name="Iowa"><name sortKey="Jia, Hong Peng" sort="Jia, Hong Peng" uniqKey="Jia H" first="Hong Peng" last="Jia">Hong Peng Jia</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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