Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro.
Identifieur interne : 002329 ( PubMed/Corpus ); précédent : 002328; suivant : 002330Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro.
Auteurs : Yu-Ting Yen ; Fang Liao ; Cheng-Hsiang Hsiao ; Chuan-Liang Kao ; Yee-Chun Chen ; Betty A. Wu-HsiehSource :
- Journal of virology [ 0022-538X ] ; 2006.
English descriptors
- KwdEn :
- Acute Disease, Animals, Cell Adhesion Molecules (metabolism), Cell Line, Chemokines (metabolism), Epithelial Cells (immunology), Epithelial Cells (metabolism), Humans, Lectins, C-Type (metabolism), Lung (cytology), Lung (immunology), Lung (pathology), Monocytes (immunology), Monocytes (metabolism), Receptors, Cell Surface (metabolism), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (physiopathology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , metabolism : Cell Adhesion Molecules, Chemokines, Lectins, C-Type, Receptors, Cell Surface.
- cytology : Lung.
- immunology : Epithelial Cells, Lung, Monocytes, Severe Acute Respiratory Syndrome.
- metabolism : Epithelial Cells, Monocytes.
- pathogenicity : SARS Virus.
- pathology : Lung, Severe Acute Respiratory Syndrome.
- physiopathology : Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Acute Disease, Animals, Cell Line, Humans.
Abstract
The clinical picture of severe acute respiratory syndrome (SARS) is characterized by pulmonary inflammation and respiratory failure, resembling that of acute respiratory distress syndrome. However, the events that lead to the recruitment of leukocytes are poorly understood. To study the cellular response in the acute phase of SARS coronavirus (SARS-CoV)-host cell interaction, we investigated the induction of chemokines, adhesion molecules, and DC-SIGN (dendritic cell-specific ICAM-3-grabbing nonintegrin) by SARS-CoV. Immunohistochemistry revealed neutrophil, macrophage, and CD8 T-cell infiltration in the lung autopsy of a SARS patient who died during the acute phase of illness. Additionally, pneumocytes and macrophages in the patient's lung expressed P-selectin and DC-SIGN. In in vitro study, we showed that the A549 and THP-1 cell lines were susceptible to SARS-CoV. A549 cells produced CCL2/monocyte chemoattractant protein 1 (MCP-1) and CXCL8/interleukin-8 (IL-8) after interaction with SARS-CoV and expressed P-selectin and VCAM-1. Moreover, SARS-CoV induced THP-1 cells to express CCL2/MCP-1, CXCL8/IL-8, CCL3/MIP-1alpha, CXCL10/IP-10, CCL4/MIP-1beta, and CCL5/RANTES, which attracted neutrophils, monocytes, and activated T cells in a chemotaxis assay. We also demonstrated that DC-SIGN was inducible in THP-1 as well as A549 cells after SARS-CoV infection. Our in vitro experiments modeling infection in humans together with the study of a lung biopsy of a patient who died during the early phase of infection demonstrated that SARS-CoV, through a dynamic interaction with lung epithelial cells and monocytic cells, creates an environment conducive for immune cell migration and accumulation that eventually leads to lung injury.
DOI: 10.1128/JVI.80.6.2684-2693.2006
PubMed: 16501078
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Wu-Hsieh</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="RBID">pubmed:16501078</idno><idno type="pmid">16501078</idno><idno type="doi">10.1128/JVI.80.6.2684-2693.2006</idno><idno type="wicri:Area/PubMed/Corpus">002329</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002329</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro.</title><author><name sortKey="Yen, Yu Ting" sort="Yen, Yu Ting" uniqKey="Yen Y" first="Yu-Ting" last="Yen">Yu-Ting Yen</name><affiliation><nlm:affiliation>Graduate Institute of Immunology, College of Medicine, National Taiwan University, No. 1 Jen-Ai Road, Section 1, Taipei 10051, Taiwan.</nlm:affiliation></affiliation></author><author><name sortKey="Liao, Fang" sort="Liao, Fang" uniqKey="Liao F" first="Fang" last="Liao">Fang Liao</name></author><author><name sortKey="Hsiao, Cheng Hsiang" sort="Hsiao, Cheng Hsiang" uniqKey="Hsiao C" first="Cheng-Hsiang" last="Hsiao">Cheng-Hsiang Hsiao</name></author><author><name sortKey="Kao, Chuan Liang" sort="Kao, Chuan Liang" uniqKey="Kao C" first="Chuan-Liang" last="Kao">Chuan-Liang Kao</name></author><author><name sortKey="Chen, Yee Chun" sort="Chen, Yee Chun" uniqKey="Chen Y" first="Yee-Chun" last="Chen">Yee-Chun Chen</name></author><author><name sortKey="Wu Hsieh, Betty A" sort="Wu Hsieh, Betty A" uniqKey="Wu Hsieh B" first="Betty A" last="Wu-Hsieh">Betty A. Wu-Hsieh</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Cell Adhesion Molecules (metabolism)</term><term>Cell Line</term><term>Chemokines (metabolism)</term><term>Epithelial Cells (immunology)</term><term>Epithelial Cells (metabolism)</term><term>Humans</term><term>Lectins, C-Type (metabolism)</term><term>Lung (cytology)</term><term>Lung (immunology)</term><term>Lung (pathology)</term><term>Monocytes (immunology)</term><term>Monocytes (metabolism)</term><term>Receptors, Cell Surface (metabolism)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Severe Acute Respiratory Syndrome (physiopathology)</term><term>Severe Acute Respiratory Syndrome (virology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cell Adhesion Molecules</term><term>Chemokines</term><term>Lectins, C-Type</term><term>Receptors, Cell Surface</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Epithelial Cells</term><term>Lung</term><term>Monocytes</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>Monocytes</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Cell Line</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical picture of severe acute respiratory syndrome (SARS) is characterized by pulmonary inflammation and respiratory failure, resembling that of acute respiratory distress syndrome. However, the events that lead to the recruitment of leukocytes are poorly understood. To study the cellular response in the acute phase of SARS coronavirus (SARS-CoV)-host cell interaction, we investigated the induction of chemokines, adhesion molecules, and DC-SIGN (dendritic cell-specific ICAM-3-grabbing nonintegrin) by SARS-CoV. Immunohistochemistry revealed neutrophil, macrophage, and CD8 T-cell infiltration in the lung autopsy of a SARS patient who died during the acute phase of illness. Additionally, pneumocytes and macrophages in the patient's lung expressed P-selectin and DC-SIGN. In in vitro study, we showed that the A549 and THP-1 cell lines were susceptible to SARS-CoV. A549 cells produced CCL2/monocyte chemoattractant protein 1 (MCP-1) and CXCL8/interleukin-8 (IL-8) after interaction with SARS-CoV and expressed P-selectin and VCAM-1. Moreover, SARS-CoV induced THP-1 cells to express CCL2/MCP-1, CXCL8/IL-8, CCL3/MIP-1alpha, CXCL10/IP-10, CCL4/MIP-1beta, and CCL5/RANTES, which attracted neutrophils, monocytes, and activated T cells in a chemotaxis assay. We also demonstrated that DC-SIGN was inducible in THP-1 as well as A549 cells after SARS-CoV infection. Our in vitro experiments modeling infection in humans together with the study of a lung biopsy of a patient who died during the early phase of infection demonstrated that SARS-CoV, through a dynamic interaction with lung epithelial cells and monocytic cells, creates an environment conducive for immune cell migration and accumulation that eventually leads to lung injury.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16501078</PMID><DateCompleted><Year>2006</Year><Month>04</Month><Day>05</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>80</Volume><Issue>6</Issue><PubDate><Year>2006</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro.</ArticleTitle><Pagination><MedlinePgn>2684-93</MedlinePgn></Pagination><Abstract><AbstractText>The clinical picture of severe acute respiratory syndrome (SARS) is characterized by pulmonary inflammation and respiratory failure, resembling that of acute respiratory distress syndrome. However, the events that lead to the recruitment of leukocytes are poorly understood. To study the cellular response in the acute phase of SARS coronavirus (SARS-CoV)-host cell interaction, we investigated the induction of chemokines, adhesion molecules, and DC-SIGN (dendritic cell-specific ICAM-3-grabbing nonintegrin) by SARS-CoV. Immunohistochemistry revealed neutrophil, macrophage, and CD8 T-cell infiltration in the lung autopsy of a SARS patient who died during the acute phase of illness. Additionally, pneumocytes and macrophages in the patient's lung expressed P-selectin and DC-SIGN. In in vitro study, we showed that the A549 and THP-1 cell lines were susceptible to SARS-CoV. A549 cells produced CCL2/monocyte chemoattractant protein 1 (MCP-1) and CXCL8/interleukin-8 (IL-8) after interaction with SARS-CoV and expressed P-selectin and VCAM-1. Moreover, SARS-CoV induced THP-1 cells to express CCL2/MCP-1, CXCL8/IL-8, CCL3/MIP-1alpha, CXCL10/IP-10, CCL4/MIP-1beta, and CCL5/RANTES, which attracted neutrophils, monocytes, and activated T cells in a chemotaxis assay. We also demonstrated that DC-SIGN was inducible in THP-1 as well as A549 cells after SARS-CoV infection. Our in vitro experiments modeling infection in humans together with the study of a lung biopsy of a patient who died during the early phase of infection demonstrated that SARS-CoV, through a dynamic interaction with lung epithelial cells and monocytic cells, creates an environment conducive for immune cell migration and accumulation that eventually leads to lung injury.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yen</LastName><ForeName>Yu-Ting</ForeName><Initials>YT</Initials><AffiliationInfo><Affiliation>Graduate Institute of Immunology, College of Medicine, National Taiwan University, No. 1 Jen-Ai Road, Section 1, Taipei 10051, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liao</LastName><ForeName>Fang</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Hsiao</LastName><ForeName>Cheng-Hsiang</ForeName><Initials>CH</Initials></Author><Author 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IdType="pubmed">10893199</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Med Res. 2005 Mar 29;10(3):117-20</Citation><ArticleIdList><ArticleId IdType="pubmed">15851378</ArticleId></ArticleIdList></Reference><Reference><Citation>J Leukoc Biol. 2002 Mar;71(3):445-57</Citation><ArticleIdList><ArticleId IdType="pubmed">11867682</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1986-94</Citation><ArticleIdList><ArticleId IdType="pubmed">12682352</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2003 May 24;361(9371):1767-72</Citation><ArticleIdList><ArticleId IdType="pubmed">12781535</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2003 May 24;361(9371):1773-8</Citation><ArticleIdList><ArticleId IdType="pubmed">12781536</ArticleId></ArticleIdList></Reference><Reference><Citation>Microcirculation. 2003 Jun;10(3-4):273-88</Citation><ArticleIdList><ArticleId IdType="pubmed">12851645</ArticleId></ArticleIdList></Reference><Reference><Citation>Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2003 Jun;25(3):360-2</Citation><ArticleIdList><ArticleId IdType="pubmed">12905758</ArticleId></ArticleIdList></Reference><Reference><Citation>Hum Pathol. 2003 Aug;34(8):743-8</Citation><ArticleIdList><ArticleId IdType="pubmed">14506633</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2003 Sep;9(9):1163-7</Citation><ArticleIdList><ArticleId IdType="pubmed">14519257</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Biol. 2003 Dec 8;163(5):1145-55</Citation><ArticleIdList><ArticleId IdType="pubmed">14662752</ArticleId></ArticleIdList></Reference><Reference><Citation>J Pathol. 2004 Feb;202(2):157-63</Citation><ArticleIdList><ArticleId IdType="pubmed">14743497</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Exp Immunol. 2004 Apr;136(1):11-2</Citation><ArticleIdList><ArticleId IdType="pubmed">15030507</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Exp Immunol. 2004 Apr;136(1):95-103</Citation><ArticleIdList><ArticleId IdType="pubmed">15030519</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2004 Feb;10(2):287-93</Citation><ArticleIdList><ArticleId IdType="pubmed">15030699</ArticleId></ArticleIdList></Reference><Reference><Citation>J Pathol. 2004 Jun;203(2):729-30; author reply 730-1</Citation><ArticleIdList><ArticleId IdType="pubmed">15141389</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2004 Jun;78(11):5642-50</Citation><ArticleIdList><ArticleId IdType="pubmed">15140961</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2004 May;10(5):818-24</Citation><ArticleIdList><ArticleId IdType="pubmed">15200814</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Microbiol. 2004 Jul;42(7):3196-206</Citation><ArticleIdList><ArticleId IdType="pubmed">15243082</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2004 Jul;10(7):1213-9</Citation><ArticleIdList><ArticleId IdType="pubmed">15324540</ArticleId></ArticleIdList></Reference><Reference><Citation>J Formos Med Assoc. 2004 Oct;103(10):787-92</Citation><ArticleIdList><ArticleId IdType="pubmed">15490031</ArticleId></ArticleIdList></Reference><Reference><Citation>Blood. 1991 Aug 15;78(4):1112-6</Citation><ArticleIdList><ArticleId IdType="pubmed">1868242</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 1992 Jun;6(6):569-75</Citation><ArticleIdList><ArticleId IdType="pubmed">1534243</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 1993 Mar 13;341(8846):643-7</Citation><ArticleIdList><ArticleId IdType="pubmed">8095568</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Crit Care Med. 1995 Nov;152(5 Pt 1):1549-54</Citation><ArticleIdList><ArticleId IdType="pubmed">7582292</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Med Today. 1996 May;2(5):198-204</Citation><ArticleIdList><ArticleId IdType="pubmed">8796888</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Crit Care Med. 1996 Sep;154(3 Pt 1):602-11</Citation><ArticleIdList><ArticleId IdType="pubmed">8810593</ArticleId></ArticleIdList></Reference><Reference><Citation>Chest. 1997 May;111(5):1306-21</Citation><ArticleIdList><ArticleId IdType="pubmed">9149588</ArticleId></ArticleIdList></Reference><Reference><Citation>Hum Pathol. 2005 Mar;36(3):303-9</Citation><ArticleIdList><ArticleId IdType="pubmed">15791576</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Crit Care Med. 2005 Apr 15;171(8):850-7</Citation><ArticleIdList><ArticleId IdType="pubmed">15657466</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol Lung Cell Mol Physiol. 2001 Jan;280(1):L58-68</Citation><ArticleIdList><ArticleId 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