Cytokine Storm in COVID-19: The Current Evidence and Treatment Strategies.
Identifieur interne : 000F81 ( Main/Corpus ); précédent : 000F80; suivant : 000F82Cytokine Storm in COVID-19: The Current Evidence and Treatment Strategies.
Auteurs : Yujun Tang ; Jiajia Liu ; Dingyi Zhang ; Zhenghao Xu ; Jinjun Ji ; Chengping WenSource :
- Frontiers in immunology [ 1664-3224 ] ; 2020.
English descriptors
- KwdEn :
- Adrenal Cortex Hormones (therapeutic use), Animals (MeSH), Antibodies, Monoclonal, Humanized (pharmacology), Antibodies, Monoclonal, Humanized (therapeutic use), Antimalarials (therapeutic use), Artesunate (therapeutic use), Betacoronavirus (immunology), COVID-19 (MeSH), Coronavirus Infections (drug therapy), Coronavirus Infections (immunology), Coronavirus Infections (virology), Hemoperfusion (methods), Humans (MeSH), Hydroxychloroquine (therapeutic use), Immunoglobulins, Intravenous (therapeutic use), Interleukin-6 (antagonists & inhibitors), Interleukin-6 (metabolism), Mice (MeSH), Pandemics (MeSH), Pneumonia, Viral (drug therapy), Pneumonia, Viral (immunology), Pneumonia, Viral (virology), Programmed Cell Death 1 Receptor (antagonists & inhibitors), SARS-CoV-2 (MeSH).
- MESH :
- chemical , antagonists & inhibitors : Interleukin-6, Programmed Cell Death 1 Receptor.
- chemical , metabolism : Interleukin-6.
- chemical , pharmacology : Antibodies, Monoclonal, Humanized.
- chemical , therapeutic use : Adrenal Cortex Hormones, Antibodies, Monoclonal, Humanized, Antimalarials, Artesunate, Hydroxychloroquine, Immunoglobulins, Intravenous.
- drug therapy : Coronavirus Infections, Pneumonia, Viral.
- immunology : Betacoronavirus, Coronavirus Infections, Pneumonia, Viral.
- methods : Hemoperfusion.
- virology : Coronavirus Infections, Pneumonia, Viral.
- Animals, COVID-19, Humans, Mice, Pandemics, SARS-CoV-2.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is the pathogen that causes coronavirus disease 2019 (COVID-19). As of 25 May 2020, the outbreak of COVID-19 has caused 347,192 deaths around the world. The current evidence showed that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who are moderately ill. The high level of cytokines also indicates a poor prognosis in COVID-19. Besides, excessive infiltration of pro-inflammatory cells, mainly involving macrophages and T-helper 17 cells, has been found in lung tissues of patients with COVID-19 by postmortem examination. Recently, increasing studies indicate that the "cytokine storm" may contribute to the mortality of COVID-19. Here, we summarize the clinical and pathologic features of the cytokine storm in COVID-19. Our review shows that SARS-Cov-2 selectively induces a high level of IL-6 and results in the exhaustion of lymphocytes. The current evidence indicates that tocilizumab, an IL-6 inhibitor, is relatively effective and safe. Besides, corticosteroids, programmed cell death protein (PD)-1/PD-L1 checkpoint inhibition, cytokine-adsorption devices, intravenous immunoglobulin, and antimalarial agents could be potentially useful and reliable approaches to counteract cytokine storm in COVID-19 patients.
DOI: 10.3389/fimmu.2020.01708
PubMed: 32754163
PubMed Central: PMC7365923
Links to Exploration step
pubmed:32754163Le document en format XML
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sortKey="Xu, Zhenghao" sort="Xu, Zhenghao" uniqKey="Xu Z" first="Zhenghao" last="Xu">Zhenghao Xu</name><affiliation><nlm:affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ji, Jinjun" sort="Ji, Jinjun" uniqKey="Ji J" first="Jinjun" last="Ji">Jinjun Ji</name><affiliation><nlm:affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wen, Chengping" sort="Wen, Chengping" uniqKey="Wen C" first="Chengping" last="Wen">Chengping Wen</name><affiliation><nlm:affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32754163</idno><idno type="pmid">32754163</idno><idno 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uniqKey="Zhang D" first="Dingyi" last="Zhang">Dingyi Zhang</name><affiliation><nlm:affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</nlm:affiliation></affiliation></author><author><name sortKey="Xu, Zhenghao" sort="Xu, Zhenghao" uniqKey="Xu Z" first="Zhenghao" last="Xu">Zhenghao Xu</name><affiliation><nlm:affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ji, Jinjun" sort="Ji, Jinjun" uniqKey="Ji J" first="Jinjun" last="Ji">Jinjun Ji</name><affiliation><nlm:affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wen, Chengping" sort="Wen, Chengping" uniqKey="Wen C" first="Chengping" last="Wen">Chengping Wen</name><affiliation><nlm:affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Frontiers in immunology</title><idno type="eISSN">1664-3224</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenal Cortex Hormones (therapeutic use)</term><term>Animals (MeSH)</term><term>Antibodies, Monoclonal, Humanized (pharmacology)</term><term>Antibodies, Monoclonal, Humanized (therapeutic use)</term><term>Antimalarials (therapeutic use)</term><term>Artesunate (therapeutic use)</term><term>Betacoronavirus (immunology)</term><term>COVID-19 (MeSH)</term><term>Coronavirus Infections (drug therapy)</term><term>Coronavirus Infections (immunology)</term><term>Coronavirus Infections (virology)</term><term>Hemoperfusion (methods)</term><term>Humans (MeSH)</term><term>Hydroxychloroquine (therapeutic use)</term><term>Immunoglobulins, Intravenous (therapeutic use)</term><term>Interleukin-6 (antagonists & inhibitors)</term><term>Interleukin-6 (metabolism)</term><term>Mice (MeSH)</term><term>Pandemics (MeSH)</term><term>Pneumonia, Viral (drug therapy)</term><term>Pneumonia, Viral (immunology)</term><term>Pneumonia, Viral (virology)</term><term>Programmed Cell Death 1 Receptor (antagonists & inhibitors)</term><term>SARS-CoV-2 (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Interleukin-6</term><term>Programmed Cell Death 1 Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interleukin-6</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antibodies, Monoclonal, Humanized</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Adrenal Cortex Hormones</term><term>Antibodies, Monoclonal, Humanized</term><term>Antimalarials</term><term>Artesunate</term><term>Hydroxychloroquine</term><term>Immunoglobulins, Intravenous</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Betacoronavirus</term><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Hemoperfusion</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>COVID-19</term><term>Humans</term><term>Mice</term><term>Pandemics</term><term>SARS-CoV-2</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is the pathogen that causes coronavirus disease 2019 (COVID-19). As of 25 May 2020, the outbreak of COVID-19 has caused 347,192 deaths around the world. The current evidence showed that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who are moderately ill. The high level of cytokines also indicates a poor prognosis in COVID-19. Besides, excessive infiltration of pro-inflammatory cells, mainly involving macrophages and T-helper 17 cells, has been found in lung tissues of patients with COVID-19 by postmortem examination. Recently, increasing studies indicate that the "cytokine storm" may contribute to the mortality of COVID-19. Here, we summarize the clinical and pathologic features of the cytokine storm in COVID-19. Our review shows that SARS-Cov-2 selectively induces a high level of IL-6 and results in the exhaustion of lymphocytes. The current evidence indicates that tocilizumab, an IL-6 inhibitor, is relatively effective and safe. Besides, corticosteroids, programmed cell death protein (PD)-1/PD-L1 checkpoint inhibition, cytokine-adsorption devices, intravenous immunoglobulin, and antimalarial agents could be potentially useful and reliable approaches to counteract cytokine storm in COVID-19 patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32754163</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>21</Day></DateCompleted><DateRevised><Year>2020</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1664-3224</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>Frontiers in immunology</Title><ISOAbbreviation>Front Immunol</ISOAbbreviation></Journal><ArticleTitle>Cytokine Storm in COVID-19: The Current Evidence and Treatment Strategies.</ArticleTitle><Pagination><MedlinePgn>1708</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fimmu.2020.01708</ELocationID><Abstract><AbstractText>Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is the pathogen that causes coronavirus disease 2019 (COVID-19). As of 25 May 2020, the outbreak of COVID-19 has caused 347,192 deaths around the world. The current evidence showed that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who are moderately ill. The high level of cytokines also indicates a poor prognosis in COVID-19. Besides, excessive infiltration of pro-inflammatory cells, mainly involving macrophages and T-helper 17 cells, has been found in lung tissues of patients with COVID-19 by postmortem examination. Recently, increasing studies indicate that the "cytokine storm" may contribute to the mortality of COVID-19. Here, we summarize the clinical and pathologic features of the cytokine storm in COVID-19. Our review shows that SARS-Cov-2 selectively induces a high level of IL-6 and results in the exhaustion of lymphocytes. The current evidence indicates that tocilizumab, an IL-6 inhibitor, is relatively effective and safe. Besides, corticosteroids, programmed cell death protein (PD)-1/PD-L1 checkpoint inhibition, cytokine-adsorption devices, intravenous immunoglobulin, and antimalarial agents could be potentially useful and reliable approaches to counteract cytokine storm in COVID-19 patients.</AbstractText><CopyrightInformation>Copyright © 2020 Tang, Liu, Zhang, Xu, Ji and Wen.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Yujun</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jiajia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Dingyi</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Zhenghao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ji</LastName><ForeName>Jinjun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wen</LastName><ForeName>Chengping</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, 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