MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile.
Identifieur interne : 000859 ( PubMed/Checkpoint ); précédent : 000858; suivant : 000860MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile.
Auteurs : Waleed H. Mahallawi [Arabie saoudite] ; Omar F. Khabour [Jordanie] ; Qibo Zhang [Royaume-Uni] ; Hatim M. Makhdoum [Arabie saoudite] ; Bandar A. Suliman [Arabie saoudite]Source :
- Cytokine [ 1096-0023 ] ; 2018.
Descripteurs français
- KwdFr :
- Adulte, Adulte d'âge moyen, Cellules Th17 (métabolisme), Coronavirus du syndrome respiratoire du Moyen-Orient (physiologie), Cytokines (), Cytokines (métabolisme), Cytokines (sang), Humains, Infections à coronavirus (immunologie), Infections à coronavirus (sang), Infections à coronavirus (virologie), Interférons (métabolisme), Interférons (sang), Jeune adulte, Lymphocytes auxiliaires Th1 (métabolisme), Mâle, Structure secondaire des protéines.
- MESH :
- immunologie : Infections à coronavirus.
- métabolisme : Cellules Th17, Cytokines, Interférons, Lymphocytes auxiliaires Th1.
- physiologie : Coronavirus du syndrome respiratoire du Moyen-Orient.
- sang : Cytokines, Infections à coronavirus, Interférons.
- virologie : Infections à coronavirus.
- Adulte, Adulte d'âge moyen, Cytokines, Humains, Jeune adulte, Mâle, Structure secondaire des protéines.
English descriptors
- KwdEn :
- Adult, Coronavirus Infections (blood), Coronavirus Infections (immunology), Coronavirus Infections (virology), Cytokines (blood), Cytokines (chemistry), Cytokines (metabolism), Humans, Interferons (blood), Interferons (metabolism), Male, Middle Aged, Middle East Respiratory Syndrome Coronavirus (physiology), Protein Structure, Secondary, Th1 Cells (metabolism), Th17 Cells (metabolism), Young Adult.
- MESH :
- chemical , blood : Cytokines, Interferons.
- blood : Coronavirus Infections.
- chemical , chemistry : Cytokines.
- immunology : Coronavirus Infections.
- chemical , metabolism : Cytokines, Interferons, Th1 Cells, Th17 Cells.
- physiology : Middle East Respiratory Syndrome Coronavirus.
- virology : Coronavirus Infections.
- Adult, Humans, Male, Middle Aged, Protein Structure, Secondary, Young Adult.
Abstract
The Middle East respiratory syndrome coronavirus (MERS-CoV) has been recognized as a highly pathogenic virus to humans that infects the respiratory tract and is associated with high morbidity and mortality. Studies in animal models suggest that MERS-CoV infection induces a strong inflammatory response, which may be related to the severity of disease. Data showing the cytokine profiles in humans during the acute phase of MERS-CoV infection are limited. In this study, we have analyzed the profile of cytokine responses in plasma samples from patients with confirmed MERS-CoV infections (n = 7) compared to healthy controls (n = 13). The cytokine profiles, including T helper (Th) 1, Th2 and Th17 responses, were analyzed using cytometric bead array (CBA). A prominent pro-inflammatory Th1 and Th17 response was clearly seen in patients with MERS-CoV infection, with markedly increased concentrations of IFN-γ, TNF-α, IL-15 and IL-17 compared to controls. IL-12 expression levels showed no difference between patients with MERS-CoV infection and the healthy controls despite the significantly increased levels of IFN-α2 and IFN-γ (P < .01). No changes were observed in the levels of IL-2, IL-4, IL-5, IL-13, and TGF-α (P > .05). Our results demonstrate a marked pro-inflammatory cytokine response during the acute phase of MERS-CoV infection in humans.
DOI: 10.1016/j.cyto.2018.01.025
PubMed: 29414327
Affiliations:
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Mahallawi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia.</nlm:affiliation><country xml:lang="fr">Arabie saoudite</country><wicri:regionArea>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah</wicri:regionArea><wicri:noRegion>Madinah</wicri:noRegion></affiliation></author><author><name sortKey="Khabour, Omar F" sort="Khabour, Omar F" uniqKey="Khabour O" first="Omar F" last="Khabour">Omar F. Khabour</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia; Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, Jordan University of Science and Technology, Irbid, Jordan. 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Studies in animal models suggest that MERS-CoV infection induces a strong inflammatory response, which may be related to the severity of disease. Data showing the cytokine profiles in humans during the acute phase of MERS-CoV infection are limited. In this study, we have analyzed the profile of cytokine responses in plasma samples from patients with confirmed MERS-CoV infections (n = 7) compared to healthy controls (n = 13). The cytokine profiles, including T helper (Th) 1, Th2 and Th17 responses, were analyzed using cytometric bead array (CBA). A prominent pro-inflammatory Th1 and Th17 response was clearly seen in patients with MERS-CoV infection, with markedly increased concentrations of IFN-γ, TNF-α, IL-15 and IL-17 compared to controls. IL-12 expression levels showed no difference between patients with MERS-CoV infection and the healthy controls despite the significantly increased levels of IFN-α2 and IFN-γ (P < .01). No changes were observed in the levels of IL-2, IL-4, IL-5, IL-13, and TGF-α (P > .05). Our results demonstrate a marked pro-inflammatory cytokine response during the acute phase of MERS-CoV infection in humans.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29414327</PMID><DateCompleted><Year>2019</Year><Month>04</Month><Day>29</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0023</ISSN><JournalIssue CitedMedium="Internet"><Volume>104</Volume><PubDate><Year>2018</Year><Month>04</Month></PubDate></JournalIssue><Title>Cytokine</Title><ISOAbbreviation>Cytokine</ISOAbbreviation></Journal><ArticleTitle>MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile.</ArticleTitle><Pagination><MedlinePgn>8-13</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1043-4666(18)30038-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cyto.2018.01.025</ELocationID><Abstract><AbstractText>The Middle East respiratory syndrome coronavirus (MERS-CoV) has been recognized as a highly pathogenic virus to humans that infects the respiratory tract and is associated with high morbidity and mortality. Studies in animal models suggest that MERS-CoV infection induces a strong inflammatory response, which may be related to the severity of disease. Data showing the cytokine profiles in humans during the acute phase of MERS-CoV infection are limited. In this study, we have analyzed the profile of cytokine responses in plasma samples from patients with confirmed MERS-CoV infections (n = 7) compared to healthy controls (n = 13). The cytokine profiles, including T helper (Th) 1, Th2 and Th17 responses, were analyzed using cytometric bead array (CBA). A prominent pro-inflammatory Th1 and Th17 response was clearly seen in patients with MERS-CoV infection, with markedly increased concentrations of IFN-γ, TNF-α, IL-15 and IL-17 compared to controls. IL-12 expression levels showed no difference between patients with MERS-CoV infection and the healthy controls despite the significantly increased levels of IFN-α2 and IFN-γ (P < .01). No changes were observed in the levels of IL-2, IL-4, IL-5, IL-13, and TGF-α (P > .05). Our results demonstrate a marked pro-inflammatory cytokine response during the acute phase of MERS-CoV infection in humans.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mahallawi</LastName><ForeName>Waleed H</ForeName><Initials>WH</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khabour</LastName><ForeName>Omar F</ForeName><Initials>OF</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia; Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, Jordan University of Science and Technology, Irbid, Jordan. Electronic address: ofkhabour@taibahu.edu.sa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Qibo</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Makhdoum</LastName><ForeName>Hatim M</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suliman</LastName><ForeName>Bandar A</ForeName><Initials>BA</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia; Molecular Biomedicine Program, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>02</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cytokine</MedlineTA><NlmUniqueID>9005353</NlmUniqueID><ISSNLinking>1043-4666</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>9008-11-1</RegistryNumber><NameOfSubstance UI="D007372">Interferons</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007372" MajorTopicYN="N">Interferons</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D065207" MajorTopicYN="N">Middle East Respiratory Syndrome Coronavirus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017433" MajorTopicYN="N">Protein Structure, Secondary</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058504" MajorTopicYN="N">Th17 Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young 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