Eosinophils Promote Antiviral Immunity in Mice Infected with Influenza A Virus
Identifieur interne : 000714 ( Main/Exploration ); précédent : 000713; suivant : 000715Eosinophils Promote Antiviral Immunity in Mice Infected with Influenza A Virus
Auteurs : Amali E. Samarasinghe [États-Unis] ; Rossana C. N. Melo [Brésil] ; Susu Duan [États-Unis] ; Kim S. Lemessurier [États-Unis] ; Swantje Liedmann [États-Unis] ; Sherri L. Surman [États-Unis] ; James J. Lee [États-Unis] ; Julia L. Hurwitz [États-Unis] ; Paul G. Thomas [États-Unis] ; Jonathan A. Mccullers [États-Unis]Source :
- The Journal of Immunology Author Choice [ 0022-1767 ] ; 2017.
Descripteurs français
- KwdFr :
- Activation des lymphocytes (immunologie), Animaux, Asthme (), Asthme (immunologie), Cytométrie en flux, Granulocytes éosinophiles (immunologie), Hypersensibilité (), Hypersensibilité (immunologie), Infections à Orthomyxoviridae (), Infections à Orthomyxoviridae (immunologie), Lymphocytes T CD8+ (immunologie), Microscopie confocale, Microscopie électronique à transmission, Modèles animaux de maladie humaine, Poumon éosinophile (immunologie), Souris, Virus de la grippe A (immunologie).
- MESH :
- immunologie : Activation des lymphocytes, Asthme, Granulocytes éosinophiles, Hypersensibilité, Infections à Orthomyxoviridae, Lymphocytes T CD8+, Poumon éosinophile, Virus de la grippe A.
- Animaux, Asthme, Cytométrie en flux, Hypersensibilité, Infections à Orthomyxoviridae, Microscopie confocale, Microscopie électronique à transmission, Modèles animaux de maladie humaine, Souris.
English descriptors
- KwdEn :
- Animals, Asthma (complications), Asthma (immunology), CD8-Positive T-Lymphocytes (immunology), Disease Models, Animal, Eosinophils (immunology), Flow Cytometry, Hypersensitivity (complications), Hypersensitivity (immunology), Influenza A virus (immunology), Lymphocyte Activation (immunology), Mice, Microscopy, Confocal, Microscopy, Electron, Transmission, Orthomyxoviridae Infections (complications), Orthomyxoviridae Infections (immunology), Pulmonary Eosinophilia (immunology).
- MESH :
- complications : Asthma, Hypersensitivity, Orthomyxoviridae Infections.
- immunology : Asthma, CD8-Positive T-Lymphocytes, Eosinophils, Hypersensitivity, Influenza A virus, Lymphocyte Activation, Orthomyxoviridae Infections, Pulmonary Eosinophilia.
- Animals, Disease Models, Animal, Flow Cytometry, Mice, Microscopy, Confocal, Microscopy, Electron, Transmission.
Abstract
Eosinophils are multifunctional cells of the innate immune system linked to allergic inflammation. Asthmatics were more likely to be hospitalized but less likely to suffer severe morbidity and mortality during the 2009 influenza pandemic. These epidemiologic findings were recapitulated in a mouse model of fungal asthma wherein infection during heightened allergic inflammation was protective against influenza A virus (IAV) infection and disease. Our goal was to delineate a mechanism(s) by which allergic asthma may alleviate influenza disease outcome, focused on the hypothesis that pulmonary eosinophilia linked with allergic respiratory disease is able to promote antiviral host defenses against the influenza virus. The transfer of eosinophils from the lungs of allergen-sensitized and challenged mice into influenza virus–infected mice resulted in reduced morbidity and viral burden, improved lung compliance, and increased CD8+ T cell numbers in the airways. In vitro assays with primary or bone marrow–derived eosinophils were used to determine eosinophil responses to the virus using the laboratory strain (A/PR/08/1934) or the pandemic strain (A/CA/04/2009) of IAV. Eosinophils were susceptible to IAV infection and responded by activation, piecemeal degranulation, and upregulation of Ag presentation markers. Virus- or viral peptide–exposed eosinophils induced CD8+ T cell proliferation, activation, and effector functions. Our data suggest that eosinophils promote host cellular immunity to reduce influenza virus replication in lungs, thereby providing a novel mechanism by which hosts with allergic asthma may be protected from influenza morbidity.
Url:
DOI: 10.4049/jimmunol.1600787
PubMed: 28283567
PubMed Central: 5384374
Affiliations:
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N." last="Melo">Rossana C. N. Melo</name><affiliation wicri:level="1"><nlm:aff id="aff4">Laboratory of Cellular Biology, Federal University of Juiz de Fora, Juiz de Fora, MG 36036, Brazil;</nlm:aff><country xml:lang="fr">Brésil</country><wicri:regionArea>Laboratory of Cellular Biology, Federal University of Juiz de Fora, Juiz de Fora, MG 36036</wicri:regionArea><wicri:noRegion>MG 36036</wicri:noRegion></affiliation></author><author><name sortKey="Duan, Susu" sort="Duan, Susu" uniqKey="Duan S" first="Susu" last="Duan">Susu Duan</name><affiliation wicri:level="2"><nlm:aff wicri:cut="; and" id="aff5">Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Immunology, St. Jude Children’s Research Hospital, Memphis</wicri:cityArea></affiliation></author><author><name sortKey="Lemessurier, Kim S" sort="Lemessurier, Kim S" uniqKey="Lemessurier K" first="Kim S." last="Lemessurier">Kim S. 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Surman</name><affiliation wicri:level="2"><nlm:aff id="aff3">Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN 38105;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis</wicri:cityArea></affiliation></author><author><name sortKey="Lee, James J" sort="Lee, James J" uniqKey="Lee J" first="James J." last="Lee">James J. Lee</name><affiliation wicri:level="2"><nlm:aff id="aff6">Department of Biochemistry, Mayo Clinic, Scottsdale, AZ 85259</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Biochemistry, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Hurwitz, Julia L" sort="Hurwitz, Julia L" uniqKey="Hurwitz J" first="Julia L." last="Hurwitz">Julia L. Hurwitz</name><affiliation wicri:level="2"><nlm:aff id="aff3">Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN 38105;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis</wicri:cityArea></affiliation></author><author><name sortKey="Thomas, Paul G" sort="Thomas, Paul G" uniqKey="Thomas P" first="Paul G." last="Thomas">Paul G. Thomas</name><affiliation wicri:level="2"><nlm:aff wicri:cut="; and" id="aff5">Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Immunology, St. Jude Children’s Research Hospital, Memphis</wicri:cityArea></affiliation></author><author><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A." last="Mccullers">Jonathan A. Mccullers</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38103;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Pediatrics, University of Tennessee Health Science Center, Memphis</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="aff2">Children’s Foundation Research Institute, Memphis, TN 38103;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Children’s Foundation Research Institute, Memphis</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="aff3">Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN 38105;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis</wicri:cityArea></affiliation></author></analytic><series><title level="j">The Journal of Immunology Author Choice</title><idno type="ISSN">0022-1767</idno><idno type="eISSN">1550-6606</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Asthma (complications)</term><term>Asthma (immunology)</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>Disease Models, Animal</term><term>Eosinophils (immunology)</term><term>Flow Cytometry</term><term>Hypersensitivity (complications)</term><term>Hypersensitivity (immunology)</term><term>Influenza A virus (immunology)</term><term>Lymphocyte Activation (immunology)</term><term>Mice</term><term>Microscopy, Confocal</term><term>Microscopy, Electron, Transmission</term><term>Orthomyxoviridae Infections (complications)</term><term>Orthomyxoviridae Infections (immunology)</term><term>Pulmonary Eosinophilia (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes (immunologie)</term><term>Animaux</term><term>Asthme ()</term><term>Asthme (immunologie)</term><term>Cytométrie en flux</term><term>Granulocytes éosinophiles (immunologie)</term><term>Hypersensibilité ()</term><term>Hypersensibilité (immunologie)</term><term>Infections à Orthomyxoviridae ()</term><term>Infections à Orthomyxoviridae (immunologie)</term><term>Lymphocytes T CD8+ (immunologie)</term><term>Microscopie confocale</term><term>Microscopie électronique à transmission</term><term>Modèles animaux de maladie humaine</term><term>Poumon éosinophile (immunologie)</term><term>Souris</term><term>Virus de la grippe A (immunologie)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Asthma</term><term>Hypersensitivity</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Activation des lymphocytes</term><term>Asthme</term><term>Granulocytes éosinophiles</term><term>Hypersensibilité</term><term>Infections à Orthomyxoviridae</term><term>Lymphocytes T CD8+</term><term>Poumon éosinophile</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Asthma</term><term>CD8-Positive T-Lymphocytes</term><term>Eosinophils</term><term>Hypersensitivity</term><term>Influenza A virus</term><term>Lymphocyte Activation</term><term>Orthomyxoviridae Infections</term><term>Pulmonary Eosinophilia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Flow Cytometry</term><term>Mice</term><term>Microscopy, Confocal</term><term>Microscopy, Electron, Transmission</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Asthme</term><term>Cytométrie en flux</term><term>Hypersensibilité</term><term>Infections à Orthomyxoviridae</term><term>Microscopie confocale</term><term>Microscopie électronique à transmission</term><term>Modèles animaux de maladie humaine</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Eosinophils are multifunctional cells of the innate immune system linked to allergic inflammation. Asthmatics were more likely to be hospitalized but less likely to suffer severe morbidity and mortality during the 2009 influenza pandemic. These epidemiologic findings were recapitulated in a mouse model of fungal asthma wherein infection during heightened allergic inflammation was protective against influenza A virus (IAV) infection and disease. Our goal was to delineate a mechanism(s) by which allergic asthma may alleviate influenza disease outcome, focused on the hypothesis that pulmonary eosinophilia linked with allergic respiratory disease is able to promote antiviral host defenses against the influenza virus. The transfer of eosinophils from the lungs of allergen-sensitized and challenged mice into influenza virus–infected mice resulted in reduced morbidity and viral burden, improved lung compliance, and increased CD8<sup>+</sup> T cell numbers in the airways. In vitro assays with primary or bone marrow–derived eosinophils were used to determine eosinophil responses to the virus using the laboratory strain (A/PR/08/1934) or the pandemic strain (A/CA/04/2009) of IAV. Eosinophils were susceptible to IAV infection and responded by activation, piecemeal degranulation, and upregulation of Ag presentation markers. Virus- or viral peptide–exposed eosinophils induced CD8<sup>+</sup> T cell proliferation, activation, and effector functions. Our data suggest that eosinophils promote host cellular immunity to reduce influenza virus replication in lungs, thereby providing a novel mechanism by which hosts with allergic asthma may be protected from influenza morbidity.</p></div></front></TEI><affiliations><list><country><li>Brésil</li><li>États-Unis</li></country><region><li>Arizona</li><li>Tennessee</li></region></list><tree><country name="États-Unis"><region name="Tennessee"><name sortKey="Samarasinghe, Amali E" sort="Samarasinghe, Amali E" uniqKey="Samarasinghe A" first="Amali E." last="Samarasinghe">Amali E. Samarasinghe</name></region><name sortKey="Duan, Susu" sort="Duan, Susu" uniqKey="Duan S" first="Susu" last="Duan">Susu Duan</name><name sortKey="Hurwitz, Julia L" sort="Hurwitz, Julia L" uniqKey="Hurwitz J" first="Julia L." last="Hurwitz">Julia L. Hurwitz</name><name sortKey="Lee, James J" sort="Lee, James J" uniqKey="Lee J" first="James J." last="Lee">James J. Lee</name><name sortKey="Lemessurier, Kim S" sort="Lemessurier, Kim S" uniqKey="Lemessurier K" first="Kim S." last="Lemessurier">Kim S. Lemessurier</name><name sortKey="Lemessurier, Kim S" sort="Lemessurier, Kim S" uniqKey="Lemessurier K" first="Kim S." last="Lemessurier">Kim S. Lemessurier</name><name sortKey="Liedmann, Swantje" sort="Liedmann, Swantje" uniqKey="Liedmann S" first="Swantje" last="Liedmann">Swantje Liedmann</name><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A." last="Mccullers">Jonathan A. Mccullers</name><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A." last="Mccullers">Jonathan A. Mccullers</name><name sortKey="Mccullers, Jonathan A" sort="Mccullers, Jonathan A" uniqKey="Mccullers J" first="Jonathan A." last="Mccullers">Jonathan A. Mccullers</name><name sortKey="Samarasinghe, Amali E" sort="Samarasinghe, Amali E" uniqKey="Samarasinghe A" first="Amali E." last="Samarasinghe">Amali E. Samarasinghe</name><name sortKey="Samarasinghe, Amali E" sort="Samarasinghe, Amali E" uniqKey="Samarasinghe A" first="Amali E." last="Samarasinghe">Amali E. Samarasinghe</name><name sortKey="Surman, Sherri L" sort="Surman, Sherri L" uniqKey="Surman S" first="Sherri L." last="Surman">Sherri L. Surman</name><name sortKey="Thomas, Paul G" sort="Thomas, Paul G" uniqKey="Thomas P" first="Paul G." last="Thomas">Paul G. Thomas</name></country><country name="Brésil"><noRegion><name sortKey="Melo, Rossana C N" sort="Melo, Rossana C N" uniqKey="Melo R" first="Rossana C. N." last="Melo">Rossana C. N. Melo</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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