Influenza A virus directly modulates mouse eosinophil responses.
Identifieur interne : 000018 ( PubMed/Corpus ); précédent : 000017; suivant : 000019Influenza A virus directly modulates mouse eosinophil responses.
Auteurs : Kim S. Lemessurier ; Robert Rooney ; Hazem E. Ghoneim ; Baoming Liu ; Kui Li ; Heather S. Smallwood ; Amali E. SamarasingheSource :
- Journal of leukocyte biology [ 1938-3673 ] ; 2020.
Abstract
Allergic asthma and influenza are common respiratory diseases with a high probability of co-occurrence. During the 2009 influenza pandemic, hospitalized patients with influenza experienced lower morbidity if asthma was an underlying condition. We have previously demonstrated that acute allergic asthma protects mice from severe influenza and have implicated eosinophils in the airways of mice with allergic asthma as participants in the antiviral response. However, very little is known about how eosinophils respond to direct exposure to influenza A virus (IAV) or the microenvironment in which the viral burden is high. We hypothesized that eosinophils would dynamically respond to the presence of IAV through phenotypic, transcriptomic, and physiologic changes. Using our mouse model of acute fungal asthma and influenza, we showed that eosinophils in lymphoid tissues were responsive to IAV infection in the lungs and altered surface expression of various markers necessary for cell activation in a niche-specific manner. Siglec-F expression was altered in a subset of eosinophils after virus exposure, and those expressing high Siglec-F were more active (IL-5Rαhi CD62Llo ). While eosinophils exposed to IAV decreased their overall transcriptional activity and mitochondrial oxygen consumption, transcription of genes encoding viral recognition proteins, Ddx58 (RIG-I), Tlr3, and Ifih1 (MDA5), were up-regulated. CD8+ T cells from IAV-infected mice expanded in response to IAV PB1 peptide-pulsed eosinophils, and CpG methylation in the Tbx21 promoter was reduced in these T cells. These data offer insight into how eosinophils respond to IAV and help elucidate alternative mechanisms by which they regulate antiviral immune responses during IAV infection.
DOI: 10.1002/JLB.4MA0320-343R
PubMed: 32386457
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Influenza A virus directly modulates mouse eosinophil responses.</title><author><name sortKey="Lemessurier, Kim S" sort="Lemessurier, Kim S" uniqKey="Lemessurier K" first="Kim S" last="Lemessurier">Kim S. Lemessurier</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Rooney, Robert" sort="Rooney, Robert" uniqKey="Rooney R" first="Robert" last="Rooney">Robert Rooney</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ghoneim, Hazem E" sort="Ghoneim, Hazem E" uniqKey="Ghoneim H" first="Hazem E" last="Ghoneim">Hazem E. Ghoneim</name><affiliation><nlm:affiliation>Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Baoming" sort="Liu, Baoming" uniqKey="Liu B" first="Baoming" last="Liu">Baoming Liu</name><affiliation><nlm:affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Kui" sort="Li, Kui" uniqKey="Li K" first="Kui" last="Li">Kui Li</name><affiliation><nlm:affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Smallwood, Heather S" sort="Smallwood, Heather S" uniqKey="Smallwood H" first="Heather S" last="Smallwood">Heather S. Smallwood</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Samarasinghe, Amali E" sort="Samarasinghe, Amali E" uniqKey="Samarasinghe A" first="Amali E" last="Samarasinghe">Amali E. Samarasinghe</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32386457</idno><idno type="pmid">32386457</idno><idno type="doi">10.1002/JLB.4MA0320-343R</idno><idno type="wicri:Area/PubMed/Corpus">000018</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000018</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Influenza A virus directly modulates mouse eosinophil responses.</title><author><name sortKey="Lemessurier, Kim S" sort="Lemessurier, Kim S" uniqKey="Lemessurier K" first="Kim S" last="Lemessurier">Kim S. Lemessurier</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Rooney, Robert" sort="Rooney, Robert" uniqKey="Rooney R" first="Robert" last="Rooney">Robert Rooney</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ghoneim, Hazem E" sort="Ghoneim, Hazem E" uniqKey="Ghoneim H" first="Hazem E" last="Ghoneim">Hazem E. Ghoneim</name><affiliation><nlm:affiliation>Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Baoming" sort="Liu, Baoming" uniqKey="Liu B" first="Baoming" last="Liu">Baoming Liu</name><affiliation><nlm:affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Kui" sort="Li, Kui" uniqKey="Li K" first="Kui" last="Li">Kui Li</name><affiliation><nlm:affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Smallwood, Heather S" sort="Smallwood, Heather S" uniqKey="Smallwood H" first="Heather S" last="Smallwood">Heather S. Smallwood</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Samarasinghe, Amali E" sort="Samarasinghe, Amali E" uniqKey="Samarasinghe A" first="Amali E" last="Samarasinghe">Amali E. Samarasinghe</name><affiliation><nlm:affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of leukocyte biology</title><idno type="eISSN">1938-3673</idno><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">Allergic asthma and influenza are common respiratory diseases with a high probability of co-occurrence. During the 2009 influenza pandemic, hospitalized patients with influenza experienced lower morbidity if asthma was an underlying condition. We have previously demonstrated that acute allergic asthma protects mice from severe influenza and have implicated eosinophils in the airways of mice with allergic asthma as participants in the antiviral response. However, very little is known about how eosinophils respond to direct exposure to influenza A virus (IAV) or the microenvironment in which the viral burden is high. We hypothesized that eosinophils would dynamically respond to the presence of IAV through phenotypic, transcriptomic, and physiologic changes. Using our mouse model of acute fungal asthma and influenza, we showed that eosinophils in lymphoid tissues were responsive to IAV infection in the lungs and altered surface expression of various markers necessary for cell activation in a niche-specific manner. Siglec-F expression was altered in a subset of eosinophils after virus exposure, and those expressing high Siglec-F were more active (IL-5Rα<sup>hi</sup> CD62L<sup>lo</sup> ). While eosinophils exposed to IAV decreased their overall transcriptional activity and mitochondrial oxygen consumption, transcription of genes encoding viral recognition proteins, Ddx58 (RIG-I), Tlr3, and Ifih1 (MDA5), were up-regulated. CD8<sup>+</sup> T cells from IAV-infected mice expanded in response to IAV PB1 peptide-pulsed eosinophils, and CpG methylation in the Tbx21 promoter was reduced in these T cells. These data offer insight into how eosinophils respond to IAV and help elucidate alternative mechanisms by which they regulate antiviral immune responses during IAV infection.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32386457</PMID><DateRevised><Year>2020</Year><Month>05</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1938-3673</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>May</Month><Day>09</Day></PubDate></JournalIssue><Title>Journal of leukocyte biology</Title><ISOAbbreviation>J. Leukoc. Biol.</ISOAbbreviation></Journal><ArticleTitle>Influenza A virus directly modulates mouse eosinophil responses.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1002/JLB.4MA0320-343R</ELocationID><Abstract><AbstractText>Allergic asthma and influenza are common respiratory diseases with a high probability of co-occurrence. During the 2009 influenza pandemic, hospitalized patients with influenza experienced lower morbidity if asthma was an underlying condition. We have previously demonstrated that acute allergic asthma protects mice from severe influenza and have implicated eosinophils in the airways of mice with allergic asthma as participants in the antiviral response. However, very little is known about how eosinophils respond to direct exposure to influenza A virus (IAV) or the microenvironment in which the viral burden is high. We hypothesized that eosinophils would dynamically respond to the presence of IAV through phenotypic, transcriptomic, and physiologic changes. Using our mouse model of acute fungal asthma and influenza, we showed that eosinophils in lymphoid tissues were responsive to IAV infection in the lungs and altered surface expression of various markers necessary for cell activation in a niche-specific manner. Siglec-F expression was altered in a subset of eosinophils after virus exposure, and those expressing high Siglec-F were more active (IL-5Rα<sup>hi</sup> CD62L<sup>lo</sup> ). While eosinophils exposed to IAV decreased their overall transcriptional activity and mitochondrial oxygen consumption, transcription of genes encoding viral recognition proteins, Ddx58 (RIG-I), Tlr3, and Ifih1 (MDA5), were up-regulated. CD8<sup>+</sup> T cells from IAV-infected mice expanded in response to IAV PB1 peptide-pulsed eosinophils, and CpG methylation in the Tbx21 promoter was reduced in these T cells. These data offer insight into how eosinophils respond to IAV and help elucidate alternative mechanisms by which they regulate antiviral immune responses during IAV infection.</AbstractText><CopyrightInformation>©2020 Society for Leukocyte Biology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>LeMessurier</LastName><ForeName>Kim S</ForeName><Initials>KS</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Children's Foundation Research Institute, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rooney</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Genetics, Genomics & Informatics, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Children's Foundation Research Institute, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghoneim</LastName><ForeName>Hazem E</ForeName><Initials>HE</Initials><AffiliationInfo><Affiliation>Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbial Infection and Immunity, College of Medicine, Ohio State University, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Baoming</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pathology, Division of Medical Microbiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Kui</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smallwood</LastName><ForeName>Heather S</ForeName><Initials>HS</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Children's Foundation Research Institute, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Samarasinghe</LastName><ForeName>Amali E</ForeName><Initials>AE</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-3104-2823</Identifier><AffiliationInfo><Affiliation>Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Children's Foundation Research Institute, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI125481</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI-125483</GrantID><Acronym>NH</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI-125481</GrantID><Acronym>NH</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>05</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Leukoc Biol</MedlineTA><NlmUniqueID>8405628</NlmUniqueID><ISSNLinking>0741-5400</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">allergy</Keyword><Keyword MajorTopicYN="N">asthma</Keyword><Keyword MajorTopicYN="N">co-morbidity</Keyword><Keyword MajorTopicYN="N">flow cytometry</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>10</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>03</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>03</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>5</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>5</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32386457</ArticleId><ArticleId IdType="doi">10.1002/JLB.4MA0320-343R</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Collins PD, Marleau S, Griffiths-Johnson DA, Jose PJ, Williams TJ. 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