Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro
Identifieur interne : 000532 ( PascalFrancis/Corpus ); précédent : 000531; suivant : 000533Modeling 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.
Descripteurs français
- Pascal (Inist)
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.
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Format Inist (serveur)
NO : | PASCAL 06-0171982 INIST |
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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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<server><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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