Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: possible relevance to pathogenesis.
Identifieur interne : 002714 ( PubMed/Corpus ); précédent : 002713; suivant : 002715Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: possible relevance to pathogenesis.
Auteurs : Chung Y. Cheung ; Leo L M. Poon ; Iris H Y. Ng ; Winsie Luk ; Sin-Fun Sia ; Mavis H S. Wu ; Kwok-Hung Chan ; Kwok-Yung Yuen ; Siamon Gordon ; Yi Guan ; Joseph S M. PeirisSource :
- Journal of virology [ 0022-538X ] ; 2005.
English descriptors
- KwdEn :
- Animals, Cells, Cultured, Chemokine CCL2 (genetics), Chemokine CCL2 (metabolism), Chemokine CXCL10, Chemokines, CXC (genetics), Chemokines, CXC (metabolism), Cytokines (genetics), Cytokines (metabolism), Gene Expression Profiling, Humans, Macrophages (immunology), Macrophages (virology), Mice, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Viral Proteins (genetics), Viral Proteins (metabolism), Virus Replication.
- MESH :
- chemical , genetics : Chemokine CCL2, Chemokines, CXC, Cytokines, Viral Proteins.
- chemical , metabolism : Chemokine CCL2, Chemokines, CXC, Cytokines, Viral Proteins.
- immunology : Macrophages, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- virology : Macrophages, Severe Acute Respiratory Syndrome.
- Animals, Cells, Cultured, Chemokine CXCL10, Gene Expression Profiling, Humans, Mice, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, Virus Replication.
Abstract
The pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-beta) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-gamma-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-beta, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS.
DOI: 10.1128/JVI.79.12.7819-7826.2005
PubMed: 15919935
Links to Exploration step
pubmed:15919935Le document en format XML
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Ng</name></author><author><name sortKey="Luk, Winsie" sort="Luk, Winsie" uniqKey="Luk W" first="Winsie" last="Luk">Winsie Luk</name></author><author><name sortKey="Sia, Sin Fun" sort="Sia, Sin Fun" uniqKey="Sia S" first="Sin-Fun" last="Sia">Sin-Fun Sia</name></author><author><name sortKey="Wu, Mavis H S" sort="Wu, Mavis H S" uniqKey="Wu M" first="Mavis H S" last="Wu">Mavis H S. Wu</name></author><author><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name></author><author><name sortKey="Gordon, Siamon" sort="Gordon, Siamon" uniqKey="Gordon S" first="Siamon" last="Gordon">Siamon Gordon</name></author><author><name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name></author><author><name sortKey="Peiris, Joseph S M" sort="Peiris, Joseph S M" uniqKey="Peiris J" first="Joseph S M" last="Peiris">Joseph S M. Peiris</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15919935</idno><idno type="pmid">15919935</idno><idno type="doi">10.1128/JVI.79.12.7819-7826.2005</idno><idno type="wicri:Area/PubMed/Corpus">002714</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002714</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: possible relevance to pathogenesis.</title><author><name sortKey="Cheung, Chung Y" sort="Cheung, Chung Y" uniqKey="Cheung C" first="Chung Y" last="Cheung">Chung Y. Cheung</name><affiliation><nlm:affiliation>Department of Microbiology, University Pathology Building, Queen Mary Hospital, Pokfulam Road, Hong Kong, Special Administrative Region, People's Republic of China.</nlm:affiliation></affiliation></author><author><name sortKey="Poon, Leo L M" sort="Poon, Leo L M" uniqKey="Poon L" first="Leo L M" last="Poon">Leo L M. Poon</name></author><author><name sortKey="Ng, Iris H Y" sort="Ng, Iris H Y" uniqKey="Ng I" first="Iris H Y" last="Ng">Iris H Y. Ng</name></author><author><name sortKey="Luk, Winsie" sort="Luk, Winsie" uniqKey="Luk W" first="Winsie" last="Luk">Winsie Luk</name></author><author><name sortKey="Sia, Sin Fun" sort="Sia, Sin Fun" uniqKey="Sia S" first="Sin-Fun" last="Sia">Sin-Fun Sia</name></author><author><name sortKey="Wu, Mavis H S" sort="Wu, Mavis H S" uniqKey="Wu M" first="Mavis H S" last="Wu">Mavis H S. Wu</name></author><author><name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name></author><author><name sortKey="Yuen, Kwok Yung" sort="Yuen, Kwok Yung" uniqKey="Yuen K" first="Kwok-Yung" last="Yuen">Kwok-Yung Yuen</name></author><author><name sortKey="Gordon, Siamon" sort="Gordon, Siamon" uniqKey="Gordon S" first="Siamon" last="Gordon">Siamon Gordon</name></author><author><name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name></author><author><name sortKey="Peiris, Joseph S M" sort="Peiris, Joseph S M" uniqKey="Peiris J" first="Joseph S M" last="Peiris">Joseph S M. Peiris</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Chemokine CCL2 (genetics)</term><term>Chemokine CCL2 (metabolism)</term><term>Chemokine CXCL10</term><term>Chemokines, CXC (genetics)</term><term>Chemokines, CXC (metabolism)</term><term>Cytokines (genetics)</term><term>Cytokines (metabolism)</term><term>Gene Expression Profiling</term><term>Humans</term><term>Macrophages (immunology)</term><term>Macrophages (virology)</term><term>Mice</term><term>Oligonucleotide Array Sequence Analysis</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Viral Proteins (genetics)</term><term>Viral Proteins (metabolism)</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Chemokine CCL2</term><term>Chemokines, CXC</term><term>Cytokines</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Chemokine CCL2</term><term>Chemokines, CXC</term><term>Cytokines</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Macrophages</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Macrophages</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Chemokine CXCL10</term><term>Gene Expression Profiling</term><term>Humans</term><term>Mice</term><term>Oligonucleotide Array Sequence Analysis</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Virus Replication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-beta) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-gamma-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-beta, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15919935</PMID><DateCompleted><Year>2005</Year><Month>06</Month><Day>28</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>12</Issue><PubDate><Year>2005</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: possible relevance to pathogenesis.</ArticleTitle><Pagination><MedlinePgn>7819-26</MedlinePgn></Pagination><Abstract><AbstractText>The pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-beta) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-gamma-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-beta, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cheung</LastName><ForeName>Chung Y</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University Pathology Building, Queen Mary Hospital, Pokfulam Road, Hong Kong, Special Administrative Region, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Poon</LastName><ForeName>Leo L M</ForeName><Initials>LL</Initials></Author><Author ValidYN="Y"><LastName>Ng</LastName><ForeName>Iris H Y</ForeName><Initials>IH</Initials></Author><Author ValidYN="Y"><LastName>Luk</LastName><ForeName>Winsie</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Sia</LastName><ForeName>Sin-Fun</ForeName><Initials>SF</Initials></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Mavis H S</ForeName><Initials>MH</Initials></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Kwok-Hung</ForeName><Initials>KH</Initials></Author><Author ValidYN="Y"><LastName>Yuen</LastName><ForeName>Kwok-Yung</ForeName><Initials>KY</Initials></Author><Author ValidYN="Y"><LastName>Gordon</LastName><ForeName>Siamon</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Guan</LastName><ForeName>Yi</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Peiris</LastName><ForeName>Joseph S M</ForeName><Initials>JS</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01AI95357</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., 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