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Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)-associated coronavirus infection.

Identifieur interne : 002631 ( PubMed/Curation ); précédent : 002630; suivant : 002632

Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)-associated coronavirus infection.

Auteurs : Yao-Hsu Yang [Taïwan] ; Yu-Hui Huang ; Ya-Hui Chuang ; Chung-Min Peng ; Li-Chieh Wang ; Yu-Tsan Lin ; Bor-Luen Chiang

Source :

RBID : pubmed:16032747

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English descriptors

Abstract

The severe acute respiratory syndrome (SARS) is caused by infection with the SARS-associated coronavirus (SARS-CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell-line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell-based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti-A549 cells antibodies, IgG anti-HUVEC antibodies, and IgM anti-HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS-CoV infection and this phenomenon may indicate post-infectious cellular injury and also induce SARS-induced immunopathology.

DOI: 10.1002/jmv.20407
PubMed: 16032747

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pubmed:16032747

Le document en format XML

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<title xml:lang="en">Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)-associated coronavirus infection.</title>
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<name sortKey="Yang, Yao Hsu" sort="Yang, Yao Hsu" uniqKey="Yang Y" first="Yao-Hsu" last="Yang">Yao-Hsu Yang</name>
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<nlm:affiliation>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.</nlm:affiliation>
<country xml:lang="fr">Taïwan</country>
<wicri:regionArea>Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei</wicri:regionArea>
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<name sortKey="Huang, Yu Hui" sort="Huang, Yu Hui" uniqKey="Huang Y" first="Yu-Hui" last="Huang">Yu-Hui Huang</name>
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<name sortKey="Chuang, Ya Hui" sort="Chuang, Ya Hui" uniqKey="Chuang Y" first="Ya-Hui" last="Chuang">Ya-Hui Chuang</name>
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<name sortKey="Peng, Chung Min" sort="Peng, Chung Min" uniqKey="Peng C" first="Chung-Min" last="Peng">Chung-Min Peng</name>
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<name sortKey="Wang, Li Chieh" sort="Wang, Li Chieh" uniqKey="Wang L" first="Li-Chieh" last="Wang">Li-Chieh Wang</name>
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<name sortKey="Lin, Yu Tsan" sort="Lin, Yu Tsan" uniqKey="Lin Y" first="Yu-Tsan" last="Lin">Yu-Tsan Lin</name>
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<name sortKey="Chiang, Bor Luen" sort="Chiang, Bor Luen" uniqKey="Chiang B" first="Bor-Luen" last="Chiang">Bor-Luen Chiang</name>
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<term>Cell Line</term>
<term>Endothelial Cells (drug effects)</term>
<term>Enzyme-Linked Immunosorbent Assay</term>
<term>Epithelial Cells (drug effects)</term>
<term>Humans</term>
<term>Immunoglobulin A (blood)</term>
<term>Immunoglobulin G (blood)</term>
<term>Immunoglobulin M (blood)</term>
<term>Nucleocapsid Proteins (immunology)</term>
<term>SARS Virus (immunology)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
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<term>Adulte</term>
<term>Anticorps antiviraux (sang)</term>
<term>Autoanticorps (pharmacologie)</term>
<term>Cellules endothéliales ()</term>
<term>Cellules épithéliales ()</term>
<term>Humains</term>
<term>Immunoglobuline A (sang)</term>
<term>Immunoglobuline G (sang)</term>
<term>Immunoglobuline M (sang)</term>
<term>Lignée cellulaire</term>
<term>Protéines nucléocapside (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Test ELISA</term>
<term>Virus du SRAS (immunologie)</term>
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<term>Immunoglobulin A</term>
<term>Immunoglobulin G</term>
<term>Immunoglobulin M</term>
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<term>Nucleocapsid Proteins</term>
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<term>Autoantibodies</term>
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<term>Endothelial Cells</term>
<term>Epithelial Cells</term>
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<term>Protéines nucléocapside</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<term>Severe Acute Respiratory Syndrome</term>
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<term>Autoanticorps</term>
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<term>Adulte</term>
<term>Cellules endothéliales</term>
<term>Cellules épithéliales</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
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<front>
<div type="abstract" xml:lang="en">The severe acute respiratory syndrome (SARS) is caused by infection with the SARS-associated coronavirus (SARS-CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell-line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell-based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti-A549 cells antibodies, IgG anti-HUVEC antibodies, and IgM anti-HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS-CoV infection and this phenomenon may indicate post-infectious cellular injury and also induce SARS-induced immunopathology.</div>
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<AbstractText>The severe acute respiratory syndrome (SARS) is caused by infection with the SARS-associated coronavirus (SARS-CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell-line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell-based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti-A549 cells antibodies, IgG anti-HUVEC antibodies, and IgM anti-HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS-CoV infection and this phenomenon may indicate post-infectious cellular injury and also induce SARS-induced immunopathology.</AbstractText>
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