Epigenetic dysregulation of ACE2 and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients
Identifieur interne : 000838 ( Pmc/Curation ); précédent : 000837; suivant : 000839Epigenetic dysregulation of ACE2 and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients
Auteurs : Amr H. Sawalha [États-Unis] ; Ming Zhao [République populaire de Chine] ; Patrick Coit [États-Unis] ; Qianjin Lu [République populaire de Chine]Source :
- Clinical Immunology (Orlando, Fla.) [ 1521-6616 ] ; 2020.
Abstract
Infection caused by SARS-CoV-2 can result in severe respiratory complications and death. Patients with a compromised immune system are expected to be more susceptible to a severe disease course. In this report we suggest that patients with systemic lupus erythematous might be especially prone to severe COVID-19 independent of their immunosuppressed state from lupus treatment. Specifically, we provide evidence in lupus to suggest hypomethylation and overexpression of
Url:
DOI: 10.1016/j.clim.2020.108410
PubMed: 32276140
PubMed Central: 7139239
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Sawalha</name><affiliation wicri:level="1"><nlm:aff id="af0005">Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0010">Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0015">Lupus Center of Excellence, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Lupus Center of Excellence, University of Pittsburgh School of Medicine, Pittsburgh, PA</wicri:regionArea></affiliation></author><author><name sortKey="Zhao, Ming" sort="Zhao, Ming" uniqKey="Zhao M" first="Ming" last="Zhao">Ming Zhao</name><affiliation wicri:level="1"><nlm:aff id="af0020">Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0025">Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation></author><author><name sortKey="Coit, Patrick" sort="Coit, Patrick" uniqKey="Coit P" first="Patrick" last="Coit">Patrick Coit</name><affiliation wicri:level="1"><nlm:aff id="af0005">Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0030">Graduate Immunology Program, University of Michigan School of Medicine, Ann Arbor, MI, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Graduate Immunology Program, University of Michigan School of Medicine, Ann Arbor, MI</wicri:regionArea></affiliation></author><author><name sortKey="Lu, Qianjin" sort="Lu, Qianjin" uniqKey="Lu Q" first="Qianjin" last="Lu">Qianjin Lu</name><affiliation wicri:level="1"><nlm:aff id="af0020">Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0025">Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32276140</idno><idno type="pmc">7139239</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139239</idno><idno type="RBID">PMC:7139239</idno><idno type="doi">10.1016/j.clim.2020.108410</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000838</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000838</idno><idno type="wicri:Area/Pmc/Curation">000838</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000838</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Epigenetic dysregulation of <italic>ACE2</italic> and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients</title><author><name sortKey="Sawalha, Amr H" sort="Sawalha, Amr H" uniqKey="Sawalha A" first="Amr H." last="Sawalha">Amr H. Sawalha</name><affiliation wicri:level="1"><nlm:aff id="af0005">Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0010">Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0015">Lupus Center of Excellence, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Lupus Center of Excellence, University of Pittsburgh School of Medicine, Pittsburgh, PA</wicri:regionArea></affiliation></author><author><name sortKey="Zhao, Ming" sort="Zhao, Ming" uniqKey="Zhao M" first="Ming" last="Zhao">Ming Zhao</name><affiliation wicri:level="1"><nlm:aff id="af0020">Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0025">Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation></author><author><name sortKey="Coit, Patrick" sort="Coit, Patrick" uniqKey="Coit P" first="Patrick" last="Coit">Patrick Coit</name><affiliation wicri:level="1"><nlm:aff id="af0005">Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0030">Graduate Immunology Program, University of Michigan School of Medicine, Ann Arbor, MI, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Graduate Immunology Program, University of Michigan School of Medicine, Ann Arbor, MI</wicri:regionArea></affiliation></author><author><name sortKey="Lu, Qianjin" sort="Lu, Qianjin" uniqKey="Lu Q" first="Qianjin" last="Lu">Qianjin Lu</name><affiliation wicri:level="1"><nlm:aff id="af0020">Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af0025">Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan</wicri:regionArea></affiliation></author></analytic><series><title level="j">Clinical Immunology (Orlando, Fla.)</title><idno type="ISSN">1521-6616</idno><idno type="eISSN">1521-7035</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Infection caused by SARS-CoV-2 can result in severe respiratory complications and death. Patients with a compromised immune system are expected to be more susceptible to a severe disease course. In this report we suggest that patients with systemic lupus erythematous might be especially prone to severe COVID-19 independent of their immunosuppressed state from lupus treatment. Specifically, we provide evidence in lupus to suggest hypomethylation and overexpression of <italic>ACE2</italic>, which is located on the X chromosome and encodes a functional receptor for the SARS-CoV-2 spike glycoprotein. Oxidative stress induced by viral infections exacerbates the DNA methylation defect in lupus, possibly resulting in further <italic>ACE2</italic> hypomethylation and enhanced viremia. In addition, demethylation of interferon-regulated genes, NFκB, and key cytokine genes in lupus patients might exacerbate the immune response to SARS-CoV-2 and increase the likelihood of cytokine storm. These arguments suggest that inherent epigenetic dysregulation in lupus might facilitate viral entry, viremia, and an excessive immune response to SARS-CoV-2. Further, maintaining disease remission in lupus patients is critical to prevent a vicious cycle of demethylation and increased oxidative stress, which will exacerbate susceptibility to SARS-CoV-2 infection during the current pandemic. Epigenetic control of the <italic>ACE2</italic> gene might be a target for prevention and therapy in COVID-19.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Huang, C" uniqKey="Huang C">C. Huang</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y. Wang</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Ren, L" uniqKey="Ren L">L. Ren</name></author><author><name sortKey="Zhao, J" uniqKey="Zhao J">J. Zhao</name></author><author><name sortKey="Hu, Y" uniqKey="Hu Y">Y. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Clin Immunol</journal-id><journal-id journal-id-type="iso-abbrev">Clin. Immunol</journal-id><journal-title-group><journal-title>Clinical Immunology (Orlando, Fla.)</journal-title></journal-title-group><issn pub-type="ppub">1521-6616</issn><issn pub-type="epub">1521-7035</issn><publisher><publisher-name>Elsevier Inc.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32276140</article-id><article-id pub-id-type="pmc">7139239</article-id><article-id pub-id-type="publisher-id">S1521-6616(20)30239-4</article-id><article-id pub-id-type="doi">10.1016/j.clim.2020.108410</article-id><article-id pub-id-type="publisher-id">108410</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Epigenetic dysregulation of <italic>ACE2</italic> and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients</article-title></title-group><contrib-group><contrib contrib-type="author" id="au0005"><name><surname>Sawalha</surname><given-names>Amr H.</given-names></name><email>asawalha@pitt.edu</email><xref rid="af0005" ref-type="aff">a</xref><xref rid="af0010" ref-type="aff">b</xref><xref rid="af0015" ref-type="aff">c</xref><xref rid="cr0005" ref-type="corresp">⁎</xref></contrib><contrib contrib-type="author" id="au0010"><name><surname>Zhao</surname><given-names>Ming</given-names></name><xref rid="af0020" ref-type="aff">d</xref><xref rid="af0025" ref-type="aff">e</xref></contrib><contrib contrib-type="author" id="au0015"><name><surname>Coit</surname><given-names>Patrick</given-names></name><xref rid="af0005" ref-type="aff">a</xref><xref rid="af0030" ref-type="aff">f</xref></contrib><contrib contrib-type="author" id="au0020"><name><surname>Lu</surname><given-names>Qianjin</given-names></name><xref rid="af0020" ref-type="aff">d</xref><xref rid="af0025" ref-type="aff">e</xref></contrib></contrib-group><aff id="af0005"><label>a</label>Division of Rheumatology, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA, USA</aff><aff id="af0010"><label>b</label>Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA</aff><aff id="af0015"><label>c</label>Lupus Center of Excellence, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA</aff><aff id="af0020"><label>d</label>Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</aff><aff id="af0025"><label>e</label>Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China</aff><aff id="af0030"><label>f</label>Graduate Immunology Program, University of Michigan School of Medicine, Ann Arbor, MI, USA</aff><author-notes><corresp id="cr0005"><label>⁎</label>Corresponding author at: 7123 Rangos Research Center, 4401 Penn Avenue, Pittsburgh, PA 15224, USA. <email>asawalha@pitt.edu</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>8</day><month>4</month><year>2020</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>6</month><year>2020</year></pub-date><pub-date pub-type="epub"><day>8</day><month>4</month><year>2020</year></pub-date><volume>215</volume><fpage>108410</fpage><lpage>108410</lpage><history><date date-type="received"><day>1</day><month>4</month><year>2020</year></date><date date-type="rev-recd"><day>4</day><month>4</month><year>2020</year></date><date date-type="accepted"><day>4</day><month>4</month><year>2020</year></date></history><permissions><copyright-statement>© 2020 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2020</copyright-year><copyright-holder>Elsevier Inc.</copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="ab0005"><p>Infection caused by SARS-CoV-2 can result in severe respiratory complications and death. Patients with a compromised immune system are expected to be more susceptible to a severe disease course. In this report we suggest that patients with systemic lupus erythematous might be especially prone to severe COVID-19 independent of their immunosuppressed state from lupus treatment. Specifically, we provide evidence in lupus to suggest hypomethylation and overexpression of <italic>ACE2</italic>, which is located on the X chromosome and encodes a functional receptor for the SARS-CoV-2 spike glycoprotein. Oxidative stress induced by viral infections exacerbates the DNA methylation defect in lupus, possibly resulting in further <italic>ACE2</italic> hypomethylation and enhanced viremia. In addition, demethylation of interferon-regulated genes, NFκB, and key cytokine genes in lupus patients might exacerbate the immune response to SARS-CoV-2 and increase the likelihood of cytokine storm. These arguments suggest that inherent epigenetic dysregulation in lupus might facilitate viral entry, viremia, and an excessive immune response to SARS-CoV-2. Further, maintaining disease remission in lupus patients is critical to prevent a vicious cycle of demethylation and increased oxidative stress, which will exacerbate susceptibility to SARS-CoV-2 infection during the current pandemic. Epigenetic control of the <italic>ACE2</italic> gene might be a target for prevention and therapy in COVID-19.</p></abstract><abstract abstract-type="author-highlights" id="ab0010"><title>Highlights</title><p><list list-type="simple" id="l0005"><list-item id="li0005"><label>•</label><p id="p0005"><italic>ACE2</italic> encodes a key viral entry receptor for SARS-CoV-2 and is methylation sensitive</p></list-item><list-item id="li0010"><label>•</label><p id="p0010"><italic>ACE2</italic> is hypomethylated and overexpressed in lupus T cells suggesting an increased possibility of disseminated disease during SARS-CoV-2 infection</p></list-item><list-item id="li0015"><label>•</label><p id="p0015"><italic>ACE2</italic> demethylation might be exacerbated after SARS-CoV-2 infection due to increased oxidative stress</p></list-item><list-item id="li0020"><label>•</label><p id="p0020">Demethylation in interferon-regulated and key cytokine genes might predispose lupus patients to cytokine storm in COVID-19</p></list-item><list-item id="li0025"><label>•</label><p id="p0025">Maintaining remission in lupus is critical to prevent further demethylation and overexpression of <italic>ACE2</italic></p></list-item></list></p></abstract><kwd-group id="ks0005"><title>Keywords</title><kwd>SARS-CoV-2</kwd><kwd>Lupus</kwd><kwd>COVID-19</kwd><kwd>Epigenetics</kwd><kwd>ACE2</kwd><kwd>Methylation</kwd><kwd>Interferon</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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