Natural Killer cell activation, reduced ACE2, TMPRSS2, cytokines G-CSF, M-CSF and SARS-CoV-2-S pseudovirus infectivity by MEK inhibitor treatment of human cells.
Identifieur interne : 000E91 ( Main/Corpus ); précédent : 000E90; suivant : 000E92Natural Killer cell activation, reduced ACE2, TMPRSS2, cytokines G-CSF, M-CSF and SARS-CoV-2-S pseudovirus infectivity by MEK inhibitor treatment of human cells.
Auteurs : Lanlan Zhou ; Kelsey Huntington ; Shengliang Zhang ; Lindsey Carlsen ; Eui-Young So ; Cassandra Parker ; Ilyas Sahin ; Howard Safran ; Suchitra Kamle ; Chang-Min Lee ; Chun Geun Lee ; Jack A. Elias ; Kerry S. Campbell ; Mandar T. Naik ; Walter J. Atwood ; Emile Youssef ; Jonathan A. Pachter ; Arunasalam Navaraj ; Attila A. Seyhan ; Olin Liang ; Wafik S. El-DeirySource :
- bioRxiv : the preprint server for biology ; 2020.
Abstract
COVID-19 affects vulnerable populations including elderly individuals and patients with cancer. Natural Killer (NK) cells and innate-immune TRAIL suppress transformed and virally-infected cells. ACE2, and TMPRSS2 protease promote SARS-CoV-2 infectivity, while inflammatory cytokines IL-6, or G-CSF worsen COVID-19 severity. We show MEK inhibitors (MEKi) VS-6766, trametinib and selumetinib reduce ACE2 expression in human cells. Chloroquine or hydroxychloroquine increase cleaved active SP-domain of TMPRSS2, and this is potentiated by MEKi. In some human cells, remdesivir increases ACE2-promoter luciferase-reporter expression, ACE2 mRNA and protein, and ACE2 expression is attenuated by MEKi. We show elevated cytokines in COVID-19- (+) patient plasma (N=9) versus control (N=11). TMPRSS2, inflammatory cytokines G-CSF, M- CSF, IL-1a, IL-6 and MCP-1 are suppressed by MEKi alone or in combination with remdesivir. MEKi enhance NK cell (but not T-cell) killing of target-cells, without suppressing TRAIL-mediated cytotoxicity. We generated a pseudotyped SARS-CoV-2 virus with a lentiviral core but with the SARS-CoV-2 D614 or G614 SPIKE (S) protein on its envelope and used VSV-G lentivirus as a negative control. Our results show infection of human bronchial epithelial cells or lung cancer cells and that MEKi suppress infectivity of the SARS-CoV-2-S pseudovirus following infection. We show a drug class-effect with MEKi to promote immune responses involving NK cells, inhibit inflammatory cytokines and block host-factors for SARS-CoV-2 infection leading also to suppression of SARS-CoV-2-S pseudovirus infection of human cells in a model system. MEKi may attenuate coronavirus infection to allow immune responses and antiviral agents to control COVID-19 disease progression and severity.
DOI: 10.1101/2020.08.02.230839
PubMed: 32793908
PubMed Central: PMC7418728
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El-Deiry</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32793908</idno><idno type="pmid">32793908</idno><idno type="doi">10.1101/2020.08.02.230839</idno><idno type="pmc">PMC7418728</idno><idno type="wicri:Area/Main/Corpus">000E91</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000E91</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Natural Killer cell activation, reduced ACE2, TMPRSS2, cytokines G-CSF, M-CSF and SARS-CoV-2-S pseudovirus infectivity by MEK inhibitor treatment of human cells.</title><author><name sortKey="Zhou, Lanlan" sort="Zhou, Lanlan" uniqKey="Zhou L" first="Lanlan" last="Zhou">Lanlan Zhou</name></author><author><name sortKey="Huntington, Kelsey" sort="Huntington, Kelsey" uniqKey="Huntington K" first="Kelsey" last="Huntington">Kelsey Huntington</name></author><author><name sortKey="Zhang, Shengliang" sort="Zhang, Shengliang" uniqKey="Zhang S" first="Shengliang" last="Zhang">Shengliang Zhang</name></author><author><name sortKey="Carlsen, Lindsey" sort="Carlsen, Lindsey" uniqKey="Carlsen L" first="Lindsey" last="Carlsen">Lindsey Carlsen</name></author><author><name sortKey="So, Eui Young" sort="So, Eui Young" uniqKey="So E" first="Eui-Young" last="So">Eui-Young So</name></author><author><name sortKey="Parker, Cassandra" sort="Parker, Cassandra" uniqKey="Parker C" first="Cassandra" last="Parker">Cassandra Parker</name></author><author><name sortKey="Sahin, Ilyas" sort="Sahin, Ilyas" uniqKey="Sahin I" first="Ilyas" last="Sahin">Ilyas Sahin</name></author><author><name sortKey="Safran, Howard" sort="Safran, Howard" uniqKey="Safran H" first="Howard" last="Safran">Howard Safran</name></author><author><name sortKey="Kamle, Suchitra" sort="Kamle, Suchitra" uniqKey="Kamle S" first="Suchitra" last="Kamle">Suchitra Kamle</name></author><author><name sortKey="Lee, Chang Min" sort="Lee, Chang Min" uniqKey="Lee C" first="Chang-Min" last="Lee">Chang-Min Lee</name></author><author><name sortKey="Lee, Chun Geun" sort="Lee, Chun Geun" uniqKey="Lee C" first="Chun Geun" last="Lee">Chun Geun Lee</name></author><author><name sortKey="Elias, Jack A" sort="Elias, Jack A" uniqKey="Elias J" first="Jack A" last="Elias">Jack A. Elias</name></author><author><name sortKey="Campbell, Kerry S" sort="Campbell, Kerry S" uniqKey="Campbell K" first="Kerry S" last="Campbell">Kerry S. Campbell</name></author><author><name sortKey="Naik, Mandar T" sort="Naik, Mandar T" uniqKey="Naik M" first="Mandar T" last="Naik">Mandar T. Naik</name></author><author><name sortKey="Atwood, Walter J" sort="Atwood, Walter J" uniqKey="Atwood W" first="Walter J" last="Atwood">Walter J. Atwood</name></author><author><name sortKey="Youssef, Emile" sort="Youssef, Emile" uniqKey="Youssef E" first="Emile" last="Youssef">Emile Youssef</name></author><author><name sortKey="Pachter, Jonathan A" sort="Pachter, Jonathan A" uniqKey="Pachter J" first="Jonathan A" last="Pachter">Jonathan A. Pachter</name></author><author><name sortKey="Navaraj, Arunasalam" sort="Navaraj, Arunasalam" uniqKey="Navaraj A" first="Arunasalam" last="Navaraj">Arunasalam Navaraj</name></author><author><name sortKey="Seyhan, Attila A" sort="Seyhan, Attila A" uniqKey="Seyhan A" first="Attila A" last="Seyhan">Attila A. Seyhan</name></author><author><name sortKey="Liang, Olin" sort="Liang, Olin" uniqKey="Liang O" first="Olin" last="Liang">Olin Liang</name></author><author><name sortKey="El Deiry, Wafik S" sort="El Deiry, Wafik S" uniqKey="El Deiry W" first="Wafik S" last="El-Deiry">Wafik S. El-Deiry</name></author></analytic><series><title level="j">bioRxiv : the preprint server for biology</title><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">COVID-19 affects vulnerable populations including elderly individuals and patients with cancer. Natural Killer (NK) cells and innate-immune TRAIL suppress transformed and virally-infected cells. ACE2, and TMPRSS2 protease promote SARS-CoV-2 infectivity, while inflammatory cytokines IL-6, or G-CSF worsen COVID-19 severity. We show MEK inhibitors (MEKi) VS-6766, trametinib and selumetinib reduce ACE2 expression in human cells. Chloroquine or hydroxychloroquine increase cleaved active SP-domain of TMPRSS2, and this is potentiated by MEKi. In some human cells, remdesivir increases ACE2-promoter luciferase-reporter expression, ACE2 mRNA and protein, and ACE2 expression is attenuated by MEKi. We show elevated cytokines in COVID-19- (+) patient plasma (N=9) versus control (N=11). TMPRSS2, inflammatory cytokines G-CSF, M- CSF, IL-1a, IL-6 and MCP-1 are suppressed by MEKi alone or in combination with remdesivir. MEKi enhance NK cell (but not T-cell) killing of target-cells, without suppressing TRAIL-mediated cytotoxicity. We generated a pseudotyped SARS-CoV-2 virus with a lentiviral core but with the SARS-CoV-2 D614 or G614 SPIKE (S) protein on its envelope and used VSV-G lentivirus as a negative control. Our results show infection of human bronchial epithelial cells or lung cancer cells and that MEKi suppress infectivity of the SARS-CoV-2-S pseudovirus following infection. We show a drug class-effect with MEKi to promote immune responses involving NK cells, inhibit inflammatory cytokines and block host-factors for SARS-CoV-2 infection leading also to suppression of SARS-CoV-2-S pseudovirus infection of human cells in a model system. MEKi may attenuate coronavirus infection to allow immune responses and antiviral agents to control COVID-19 disease progression and severity.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">32793908</PMID><DateRevised><Year>2021</Year><Month>05</Month><Day>15</Day></DateRevised><Article PubModel="Electronic"><Journal><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Aug</Month><Day>03</Day></PubDate></JournalIssue><Title>bioRxiv : the preprint server for biology</Title><ISOAbbreviation>bioRxiv</ISOAbbreviation></Journal><ArticleTitle>Natural Killer cell activation, reduced ACE2, TMPRSS2, cytokines G-CSF, M-CSF and SARS-CoV-2-S pseudovirus infectivity by MEK inhibitor treatment of human cells.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">2020.08.02.230839</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1101/2020.08.02.230839</ELocationID><Abstract><AbstractText>COVID-19 affects vulnerable populations including elderly individuals and patients with cancer. Natural Killer (NK) cells and innate-immune TRAIL suppress transformed and virally-infected cells. ACE2, and TMPRSS2 protease promote SARS-CoV-2 infectivity, while inflammatory cytokines IL-6, or G-CSF worsen COVID-19 severity. We show MEK inhibitors (MEKi) VS-6766, trametinib and selumetinib reduce ACE2 expression in human cells. Chloroquine or hydroxychloroquine increase cleaved active SP-domain of TMPRSS2, and this is potentiated by MEKi. In some human cells, remdesivir increases ACE2-promoter luciferase-reporter expression, ACE2 mRNA and protein, and ACE2 expression is attenuated by MEKi. We show elevated cytokines in COVID-19- (+) patient plasma (N=9) versus control (N=11). TMPRSS2, inflammatory cytokines G-CSF, M- CSF, IL-1a, IL-6 and MCP-1 are suppressed by MEKi alone or in combination with remdesivir. MEKi enhance NK cell (but not T-cell) killing of target-cells, without suppressing TRAIL-mediated cytotoxicity. We generated a pseudotyped SARS-CoV-2 virus with a lentiviral core but with the SARS-CoV-2 D614 or G614 SPIKE (S) protein on its envelope and used VSV-G lentivirus as a negative control. Our results show infection of human bronchial epithelial cells or lung cancer cells and that MEKi suppress infectivity of the SARS-CoV-2-S pseudovirus following infection. We show a drug class-effect with MEKi to promote immune responses involving NK cells, inhibit inflammatory cytokines and block host-factors for SARS-CoV-2 infection leading also to suppression of SARS-CoV-2-S pseudovirus infection of human cells in a model system. MEKi may attenuate coronavirus infection to allow immune responses and antiviral agents to control COVID-19 disease progression and severity.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Lanlan</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Huntington</LastName><ForeName>Kelsey</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Shengliang</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Carlsen</LastName><ForeName>Lindsey</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>So</LastName><ForeName>Eui-Young</ForeName><Initials>EY</Initials></Author><Author ValidYN="Y"><LastName>Parker</LastName><ForeName>Cassandra</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Sahin</LastName><ForeName>Ilyas</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Safran</LastName><ForeName>Howard</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Kamle</LastName><ForeName>Suchitra</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chang-Min</ForeName><Initials>CM</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chun Geun</ForeName><Initials>CG</Initials></Author><Author ValidYN="Y"><LastName>Elias</LastName><ForeName>Jack A</ForeName><Initials>JA</Initials></Author><Author ValidYN="Y"><LastName>Campbell</LastName><ForeName>Kerry S</ForeName><Initials>KS</Initials></Author><Author ValidYN="Y"><LastName>Naik</LastName><ForeName>Mandar T</ForeName><Initials>MT</Initials></Author><Author ValidYN="Y"><LastName>Atwood</LastName><ForeName>Walter J</ForeName><Initials>WJ</Initials></Author><Author ValidYN="Y"><LastName>Youssef</LastName><ForeName>Emile</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Pachter</LastName><ForeName>Jonathan A</ForeName><Initials>JA</Initials></Author><Author ValidYN="Y"><LastName>Navaraj</LastName><ForeName>Arunasalam</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Seyhan</LastName><ForeName>Attila A</ForeName><Initials>AA</Initials></Author><Author ValidYN="Y"><LastName>Liang</LastName><ForeName>Olin</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>El-Deiry</LastName><ForeName>Wafik S</ForeName><Initials>WS</Initials><Identifier Source="ORCID">0000-0002-9577-8266</Identifier></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P20 GM119943</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 GM122732</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 GM115677</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D000076942">Preprint</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>08</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>bioRxiv</MedlineTA><NlmUniqueID>101680187</NlmUniqueID></MedlineJournalInfo></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>8</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>8</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>15</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32793908</ArticleId><ArticleId 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