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Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro

Identifieur interne : 000532 ( PascalFrancis/Corpus ); précédent : 000531; suivant : 000533

Modeling 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-Hsieh

Source :

RBID : Pascal:06-0171982

Descripteurs français

English descriptors

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-1α, CXCL10/IP-10, CCL4/MIP-1β, 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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A08 01  1  ENG  @1 Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro
A11 01  1    @1 YEN (Yu-Ting)
A11 02  1    @1 FANG LIAO
A11 03  1    @1 HSIAO (Cheng-Hsiang)
A11 04  1    @1 KAO (Chuan-Liang)
A11 05  1    @1 CHEN (Yee-Chun)
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A23 01      @0 ENG
A43 01      @1 INIST @2 13592 @5 354000115204270100
A44       @0 0000 @1 © 2006 INIST-CNRS. All rights reserved.
A47 01  1    @0 06-0171982
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C01 01    ENG  @0 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-1α, CXCL10/IP-10, CCL4/MIP-1β, 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.
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Format Inist (serveur)

NO : PASCAL 06-0171982 INIST
ET : Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro
AU : YEN (Yu-Ting); FANG LIAO; HSIAO (Cheng-Hsiang); KAO (Chuan-Liang); CHEN (Yee-Chun); WU-HSIEH (Betty A.)
AF : Graduate Institute of Immunology, National Taiwan University College of Medicine/Taïwan (1 aut., 6 aut.); Institute of Biomedical Sciences, Academia Sinica/Taipei/Taïwan (2 aut.); Department of Pathology, National Taiwan University Hospital/Taïwan (3 aut.); Graduate Institute of Clinical Laboratory Sciences and Medical Biotechnology, National Taiwan University College of Medicine/Taïwan (4 aut.); Department of Internal Medicine, National Taiwan University Hospital/Taïwan (5 aut.)
DT : Publication en série; Niveau analytique
SO : Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2006; Vol. 80; No. 6; Pp. 2684-2693
LA : Anglais
EA : 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-1α, CXCL10/IP-10, CCL4/MIP-1β, 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.
CC : 002A05C10
FD : Coronavirus; Modélisation; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG : Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED : Coronavirus; Modeling; Microbiology; Virology; Severe acute respiratory syndrome
EG : Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease
SD : Coronavirus; Modelización; Microbiología; Virología; Síndrome respiratorio agudo severo
LO : INIST-13592.354000115204270100
ID : 06-0171982

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Pascal:06-0171982

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<NO>PASCAL 06-0171982 INIST</NO>
<ET>Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro</ET>
<AU>YEN (Yu-Ting); FANG LIAO; HSIAO (Cheng-Hsiang); KAO (Chuan-Liang); CHEN (Yee-Chun); WU-HSIEH (Betty A.)</AU>
<AF>Graduate Institute of Immunology, National Taiwan University College of Medicine/Taïwan (1 aut., 6 aut.); Institute of Biomedical Sciences, Academia Sinica/Taipei/Taïwan (2 aut.); Department of Pathology, National Taiwan University Hospital/Taïwan (3 aut.); Graduate Institute of Clinical Laboratory Sciences and Medical Biotechnology, National Taiwan University College of Medicine/Taïwan (4 aut.); Department of Internal Medicine, National Taiwan University Hospital/Taïwan (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2006; Vol. 80; No. 6; Pp. 2684-2693</SO>
<LA>Anglais</LA>
<EA>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-1α, CXCL10/IP-10, CCL4/MIP-1β, 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.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Modélisation; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Coronavirus; Modeling; Microbiology; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Modelización; Microbiología; Virología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000115204270100</LO>
<ID>06-0171982</ID>
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