Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection
Identifieur interne : 004F94 ( Main/Merge ); précédent : 004F93; suivant : 004F95Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection
Auteurs : Yao-Hsu Yang [Taïwan] ; Yu-Hui Huang [Taïwan] ; Ya-Hui Chuang [Taïwan] ; Chung-Min Peng [Taïwan] ; Li-Chieh Wang [Taïwan] ; Yu-Tsan Lin [Taïwan] ; Bor-Luen Chiang [Taïwan]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 2005-09.
Descripteurs français
- KwdFr :
- Adulte, Anticorps antiviraux (sang), Autoanticorps (pharmacologie), Cellules endothéliales (), Cellules épithéliales (), Humains, Immunoglobuline A (sang), Immunoglobuline G (sang), Immunoglobuline M (sang), Lignée cellulaire, Protéines nucléocapside (immunologie), Syndrome respiratoire aigu sévère (immunologie), Test ELISA, Virus du SRAS (immunologie).
- MESH :
- immunologie : Protéines nucléocapside, Syndrome respiratoire aigu sévère, Virus du SRAS.
- pharmacologie : Autoanticorps.
- sang : Anticorps antiviraux, Immunoglobuline A, Immunoglobuline G, Immunoglobuline M.
- Adulte, Cellules endothéliales, Cellules épithéliales, Humains, Lignée cellulaire, Test ELISA.
English descriptors
- KwdEn :
- Adult, Antibodies, Viral (blood), Autoantibodies (pharmacology), Cell Line, Endothelial Cells (drug effects), Enzyme-Linked Immunosorbent Assay, Epithelial Cells (drug effects), Humans, Immunoglobulin A (blood), Immunoglobulin G (blood), Immunoglobulin M (blood), Nucleocapsid Proteins (immunology), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology).
- MESH :
- chemical , blood : Antibodies, Viral, Immunoglobulin A, Immunoglobulin G, Immunoglobulin M.
- chemical , immunology : Nucleocapsid Proteins.
- chemical , pharmacology : Autoantibodies.
- drug effects : Endothelial Cells, Epithelial Cells.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- Teeft :
- Adult, Aeca, Aepca, Antibody, Assay, Autoantibody, Cell Line, Cell antibodies, Chan, Clin, Coronavirus, Cytotoxicity, Cytotoxicity index, Elisa, Endothelial, Endothelial cells, Enzyme-Linked Immunosorbent Assay, Epithelial, Epithelial cells, Healthy controls, Hpec, Human epithelial cells, Human umbilical venous, Humans, Huvec, Immunoglobulin, Indirect staining, National taiwan university hospital, Necrotizing pneumonia, Nucleocapsid protein, Peiris, Respiratory syndrome, Room temperature, Sars, Sars patients, Serum levels, Serum samples, Streptococcal necrotizing pneumonia, Syndrome, Systemic vasculitis, Test medium, Ulcerative colitis, Wang.
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. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.20407
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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. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</div>
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<profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Aeca</term>
<term>Aepca</term>
<term>Antibody</term>
<term>Assay</term>
<term>Autoantibody</term>
<term>Cell antibodies</term>
<term>Chan</term>
<term>Clin</term>
<term>Coronavirus</term>
<term>Cytotoxicity</term>
<term>Cytotoxicity index</term>
<term>Elisa</term>
<term>Endothelial</term>
<term>Endothelial cells</term>
<term>Epithelial</term>
<term>Epithelial cells</term>
<term>Healthy controls</term>
<term>Hpec</term>
<term>Human epithelial cells</term>
<term>Human umbilical venous</term>
<term>Huvec</term>
<term>Immunoglobulin</term>
<term>Indirect staining</term>
<term>National taiwan university hospital</term>
<term>Necrotizing pneumonia</term>
<term>Nucleocapsid protein</term>
<term>Peiris</term>
<term>Respiratory syndrome</term>
<term>Room temperature</term>
<term>Sars</term>
<term>Sars patients</term>
<term>Serum levels</term>
<term>Serum samples</term>
<term>Streptococcal necrotizing pneumonia</term>
<term>Syndrome</term>
<term>Systemic vasculitis</term>
<term>Test medium</term>
<term>Ulcerative colitis</term>
<term>Wang</term>
</keywords>
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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. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</div>
</front>
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<PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)-associated coronavirus infection.</title>
<author><name sortKey="Yang, Yao Hsu" sort="Yang, Yao Hsu" uniqKey="Yang Y" first="Yao-Hsu" last="Yang">Yao-Hsu Yang</name>
<affiliation wicri:level="1"><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>
<wicri:noRegion>Taipei</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Huang, Yu Hui" sort="Huang, Yu Hui" uniqKey="Huang Y" first="Yu-Hui" last="Huang">Yu-Hui Huang</name>
</author>
<author><name sortKey="Chuang, Ya Hui" sort="Chuang, Ya Hui" uniqKey="Chuang Y" first="Ya-Hui" last="Chuang">Ya-Hui Chuang</name>
</author>
<author><name sortKey="Peng, Chung Min" sort="Peng, Chung Min" uniqKey="Peng C" first="Chung-Min" last="Peng">Chung-Min Peng</name>
</author>
<author><name sortKey="Wang, Li Chieh" sort="Wang, Li Chieh" uniqKey="Wang L" first="Li-Chieh" last="Wang">Li-Chieh Wang</name>
</author>
<author><name sortKey="Lin, Yu Tsan" sort="Lin, Yu Tsan" uniqKey="Lin Y" first="Yu-Tsan" last="Lin">Yu-Tsan Lin</name>
</author>
<author><name sortKey="Chiang, Bor Luen" sort="Chiang, Bor Luen" uniqKey="Chiang B" first="Bor-Luen" last="Chiang">Bor-Luen Chiang</name>
</author>
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<date when="2005">2005</date>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)-associated coronavirus infection.</title>
<author><name sortKey="Yang, Yao Hsu" sort="Yang, Yao Hsu" uniqKey="Yang Y" first="Yao-Hsu" last="Yang">Yao-Hsu Yang</name>
<affiliation wicri:level="1"><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>
<wicri:noRegion>Taipei</wicri:noRegion>
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</author>
<author><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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<author><name sortKey="Chuang, Ya Hui" sort="Chuang, Ya Hui" uniqKey="Chuang Y" first="Ya-Hui" last="Chuang">Ya-Hui Chuang</name>
</author>
<author><name sortKey="Peng, Chung Min" sort="Peng, Chung Min" uniqKey="Peng C" first="Chung-Min" last="Peng">Chung-Min Peng</name>
</author>
<author><name sortKey="Wang, Li Chieh" sort="Wang, Li Chieh" uniqKey="Wang L" first="Li-Chieh" last="Wang">Li-Chieh Wang</name>
</author>
<author><name sortKey="Lin, Yu Tsan" sort="Lin, Yu Tsan" uniqKey="Lin Y" first="Yu-Tsan" last="Lin">Yu-Tsan Lin</name>
</author>
<author><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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<series><title level="j">Journal of medical virology</title>
<idno type="ISSN">0146-6615</idno>
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<term>Autoantibodies (pharmacology)</term>
<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>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><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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<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antibodies, Viral</term>
<term>Immunoglobulin A</term>
<term>Immunoglobulin G</term>
<term>Immunoglobulin M</term>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Autoantibodies</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Endothelial Cells</term>
<term>Epithelial Cells</term>
</keywords>
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<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<term>Immunoglobuline G</term>
<term>Immunoglobuline M</term>
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<term>Cell Line</term>
<term>Enzyme-Linked Immunosorbent Assay</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adulte</term>
<term>Cellules endothéliales</term>
<term>Cellules épithéliales</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Test ELISA</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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