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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pubmed:32386457Le document en format XML
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<author><name sortKey="Samarasinghe, Amali E" sort="Samarasinghe, Amali E" uniqKey="Samarasinghe A" first="Amali E" last="Samarasinghe">Amali E. Samarasinghe</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Influenza A virus directly modulates mouse eosinophil responses.</title>
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<author><name sortKey="Ghoneim, Hazem E" sort="Ghoneim, Hazem E" uniqKey="Ghoneim H" first="Hazem E" last="Ghoneim">Hazem E. Ghoneim</name>
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<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>
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<Month>05</Month>
<Day>18</Day>
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<Title>Journal of leukocyte biology</Title>
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<ArticleTitle>Influenza A virus directly modulates mouse eosinophil responses.</ArticleTitle>
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<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>
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<AffiliationInfo><Affiliation>Department of Genetics, Genomics & Informatics, College of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Pathology, Division of Medical Microbiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Microbiology, Immunology & Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.</Affiliation>
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