Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)-associated coronavirus infection
Identifieur interne : 000697 ( PascalFrancis/Checkpoint ); précédent : 000696; suivant : 000698Autoantibodies 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.
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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.
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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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<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>093</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations><list><country><li>Taïwan</li>
</country>
</list>
<tree><country name="Taïwan"><noRegion><name sortKey="Yang, Yao Hsu" sort="Yang, Yao Hsu" uniqKey="Yang Y" first="Yao-Hsu" last="Yang">Yao-Hsu Yang</name>
</noRegion>
<name sortKey="Chiang, Bor Luen" sort="Chiang, Bor Luen" uniqKey="Chiang B" first="Bor-Luen" last="Chiang">Bor-Luen Chiang</name>
<name sortKey="Chuang, Ya Hui" sort="Chuang, Ya Hui" uniqKey="Chuang Y" first="Ya-Hui" last="Chuang">Ya-Hui Chuang</name>
<name sortKey="Huang, Yu Hui" sort="Huang, Yu Hui" uniqKey="Huang Y" first="Yu-Hui" last="Huang">Yu-Hui Huang</name>
<name sortKey="Lin, Yu Tsan" sort="Lin, Yu Tsan" uniqKey="Lin Y" first="Yu-Tsan" last="Lin">Yu-Tsan Lin</name>
<name sortKey="Peng, Chung Min" sort="Peng, Chung Min" uniqKey="Peng C" first="Chung-Min" last="Peng">Chung-Min Peng</name>
<name sortKey="Wang, Li Chieh" sort="Wang, Li Chieh" uniqKey="Wang L" first="Li-Chieh" last="Wang">Li-Chieh Wang</name>
</country>
</tree>
</affiliations>
</record>
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