Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro.
Identifieur interne : 001398 ( Ncbi/Curation ); précédent : 001397; suivant : 001399Modeling the early events of severe acute respiratory syndrome coronavirus infection in vitro.
Auteurs : Yu-Ting Yen [Taïwan] ; Fang Liao ; Cheng-Hsiang Hsiao ; Chuan-Liang Kao ; Yee-Chun Chen ; Betty A. Wu-HsiehSource :
- Journal of virology [ 0022-538X ] ; 2006.
Descripteurs français
- KwdFr :
- Animaux, Cellules épithéliales (immunologie), Cellules épithéliales (métabolisme), Chimiokines (métabolisme), Humains, Lectines de type C (métabolisme), Lignée cellulaire, Maladie aigüe, Molécules d'adhérence cellulaire (métabolisme), Monocytes (immunologie), Monocytes (métabolisme), Poumon (anatomopathologie), Poumon (cytologie), Poumon (immunologie), Récepteurs de surface cellulaire (métabolisme), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (physiopathologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Poumon, Syndrome respiratoire aigu sévère.
- cytologie : Poumon.
- immunologie : Cellules épithéliales, Monocytes, Poumon, Syndrome respiratoire aigu sévère.
- métabolisme : Cellules épithéliales, Chimiokines, Lectines de type C, Molécules d'adhérence cellulaire, Monocytes, Récepteurs de surface cellulaire.
- pathogénicité : Virus du SRAS.
- physiopathologie : Syndrome respiratoire aigu sévère.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Humains, Lignée cellulaire, Maladie aigüe.
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></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="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules épithéliales (immunologie)</term><term>Cellules épithéliales (métabolisme)</term><term>Chimiokines (métabolisme)</term><term>Humains</term><term>Lectines de type C (métabolisme)</term><term>Lignée cellulaire</term><term>Maladie aigüe</term><term>Molécules d'adhérence cellulaire (métabolisme)</term><term>Monocytes (immunologie)</term><term>Monocytes (métabolisme)</term><term>Poumon (anatomopathologie)</term><term>Poumon (cytologie)</term><term>Poumon (immunologie)</term><term>Récepteurs de surface cellulaire (métabolisme)</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (physiopathologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Virus du SRAS (pathogénicité)</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="anatomopathologie" xml:lang="fr"><term>Poumon</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules épithéliales</term><term>Monocytes</term><term>Poumon</term><term>Syndrome respiratoire aigu sévère</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="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term><term>Chimiokines</term><term>Lectines de type C</term><term>Molécules d'adhérence cellulaire</term><term>Monocytes</term><term>Récepteurs de surface cellulaire</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</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><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Lignée cellulaire</term><term>Maladie aigüe</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></record>Pour manipuler ce document sous Unix (Dilib)
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