The immune profile associated with acute allergic asthma accelerates clearance of influenza virus.
Identifieur interne : 001F21 ( PubMed/Checkpoint ); précédent : 001F20; suivant : 001F22The immune profile associated with acute allergic asthma accelerates clearance of influenza virus.
Auteurs : Amali E. Samarasinghe [États-Unis] ; Stacie N. Woolard [États-Unis] ; Kelli L. Boyd [États-Unis] ; Scott A. Hoselton [États-Unis] ; Jane M. Schuh [États-Unis] ; Jonathan A. Mccullers [États-Unis]Source :
- Immunology and cell biology [ 1440-1711 ]
Descripteurs français
- KwdFr :
- Animaux, Asthme (immunologie), Femelle, Grippe humaine (anatomopathologie), Grippe humaine (immunologie), Grippe humaine (virologie), Humains, Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (immunologie), Infections à Orthomyxoviridae (virologie), Interactions hôte-pathogène (immunologie), Interférons (métabolisme), Maladie aigüe, Maladie chronique, Modèles animaux de maladie humaine, Muqueuse respiratoire (anatomopathologie), Muqueuse respiratoire (immunologie), Muqueuse respiratoire (virologie), Souris, Sous-type H1N1 du virus de la grippe A (immunologie).
- MESH :
- anatomopathologie : Grippe humaine, Infections à Orthomyxoviridae, Muqueuse respiratoire.
- immunologie : Asthme, Grippe humaine, Infections à Orthomyxoviridae, Interactions hôte-pathogène, Muqueuse respiratoire, Sous-type H1N1 du virus de la grippe A.
- métabolisme : Interférons.
- virologie : Grippe humaine, Infections à Orthomyxoviridae, Muqueuse respiratoire.
- Animaux, Femelle, Humains, Maladie aigüe, Maladie chronique, Modèles animaux de maladie humaine, Souris.
English descriptors
- KwdEn :
- Acute Disease, Animals, Asthma (immunology), Chronic Disease, Disease Models, Animal, Female, Host-Pathogen Interactions (immunology), Humans, Influenza A Virus, H1N1 Subtype (immunology), Influenza, Human (immunology), Influenza, Human (pathology), Influenza, Human (virology), Interferons (metabolism), Mice, Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (pathology), Orthomyxoviridae Infections (virology), Respiratory Mucosa (immunology), Respiratory Mucosa (pathology), Respiratory Mucosa (virology).
- MESH :
- chemical , metabolism : Interferons.
- immunology : Asthma, Host-Pathogen Interactions, Influenza A Virus, H1N1 Subtype, Influenza, Human, Orthomyxoviridae Infections, Respiratory Mucosa.
- pathology : Influenza, Human, Orthomyxoviridae Infections, Respiratory Mucosa.
- virology : Influenza, Human, Orthomyxoviridae Infections, Respiratory Mucosa.
- Acute Disease, Animals, Chronic Disease, Disease Models, Animal, Female, Humans, Mice.
Abstract
Asthma was the most common comorbidity in hospitalized patients during the 2009 influenza pandemic. For unknown reasons, hospitalized asthmatics had less severe outcomes and were less likely to die from pandemic influenza. Our data with primary human bronchial cells indicate that changes intrinsic to epithelial cells in asthma may protect against cytopathology induced by influenza virus. To further study influenza virus pathogenesis in allergic hosts, we aimed to develop and characterize murine models of asthma and influenza comorbidity to determine structural, physiological and immunological changes induced by influenza in the context of asthma. Aspergillus fumigatus-sensitized and -challenged C57BL/6 mice were infected with pandemic H1N1 influenza virus, either during peak allergic inflammation or during airway remodeling to gain insight into disease pathogenesis. Mice infected with the influenza virus during peak allergic inflammation did not lose body weight and cleared the virus rapidly. These mice exhibited high eosinophilia, preserved airway epithelial cell integrity, increased mucus, reduced interferon response and increased insulin-like growth factor-1. In contrast, weight loss and viral replication kinetics in the mice that were infected during the late airway remodeling phase were equivalent to flu-only controls. These mice had neutrophils in the airways, damaged airway epithelial cells, less mucus production, increased interferons and decreased insulin-like growth factor-1. The state of the allergic airways at the time of influenza virus infection alters host responses against the virus. These murine models of asthma and influenza comorbidity may improve our understanding of the epidemiology and pathogenesis of viral infections in humans with asthma.
DOI: 10.1038/icb.2013.113
PubMed: 24469764
Affiliations:
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For unknown reasons, hospitalized asthmatics had less severe outcomes and were less likely to die from pandemic influenza. Our data with primary human bronchial cells indicate that changes intrinsic to epithelial cells in asthma may protect against cytopathology induced by influenza virus. To further study influenza virus pathogenesis in allergic hosts, we aimed to develop and characterize murine models of asthma and influenza comorbidity to determine structural, physiological and immunological changes induced by influenza in the context of asthma. Aspergillus fumigatus-sensitized and -challenged C57BL/6 mice were infected with pandemic H1N1 influenza virus, either during peak allergic inflammation or during airway remodeling to gain insight into disease pathogenesis. Mice infected with the influenza virus during peak allergic inflammation did not lose body weight and cleared the virus rapidly. These mice exhibited high eosinophilia, preserved airway epithelial cell integrity, increased mucus, reduced interferon response and increased insulin-like growth factor-1. In contrast, weight loss and viral replication kinetics in the mice that were infected during the late airway remodeling phase were equivalent to flu-only controls. These mice had neutrophils in the airways, damaged airway epithelial cells, less mucus production, increased interferons and decreased insulin-like growth factor-1. The state of the allergic airways at the time of influenza virus infection alters host responses against the virus. These murine models of asthma and influenza comorbidity may improve our understanding of the epidemiology and pathogenesis of viral infections in humans with asthma. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24469764</PMID><DateCompleted><Year>2015</Year><Month>01</Month><Day>07</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1440-1711</ISSN><JournalIssue CitedMedium="Internet"><Volume>92</Volume><Issue>5</Issue><PubDate><MedlineDate>2014 May-Jun</MedlineDate></PubDate></JournalIssue><Title>Immunology and cell biology</Title><ISOAbbreviation>Immunol. Cell Biol.</ISOAbbreviation></Journal><ArticleTitle>The immune profile associated with acute allergic asthma accelerates clearance of influenza virus.</ArticleTitle><Pagination><MedlinePgn>449-59</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/icb.2013.113</ELocationID><Abstract><AbstractText>Asthma was the most common comorbidity in hospitalized patients during the 2009 influenza pandemic. For unknown reasons, hospitalized asthmatics had less severe outcomes and were less likely to die from pandemic influenza. Our data with primary human bronchial cells indicate that changes intrinsic to epithelial cells in asthma may protect against cytopathology induced by influenza virus. To further study influenza virus pathogenesis in allergic hosts, we aimed to develop and characterize murine models of asthma and influenza comorbidity to determine structural, physiological and immunological changes induced by influenza in the context of asthma. Aspergillus fumigatus-sensitized and -challenged C57BL/6 mice were infected with pandemic H1N1 influenza virus, either during peak allergic inflammation or during airway remodeling to gain insight into disease pathogenesis. Mice infected with the influenza virus during peak allergic inflammation did not lose body weight and cleared the virus rapidly. These mice exhibited high eosinophilia, preserved airway epithelial cell integrity, increased mucus, reduced interferon response and increased insulin-like growth factor-1. In contrast, weight loss and viral replication kinetics in the mice that were infected during the late airway remodeling phase were equivalent to flu-only controls. These mice had neutrophils in the airways, damaged airway epithelial cells, less mucus production, increased interferons and decreased insulin-like growth factor-1. The state of the allergic airways at the time of influenza virus infection alters host responses against the virus. These murine models of asthma and influenza comorbidity may improve our understanding of the epidemiology and pathogenesis of viral infections in humans with asthma. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Samarasinghe</LastName><ForeName>Amali E</ForeName><Initials>AE</Initials><AffiliationInfo><Affiliation>1] Department of Infectious Diseases, Memphis, TN, USA [2] St Jude Children's Research Hospital, Memphis, TN, USA [3] Department of Pediatrics, University of Tennessee Health Science Center, Children's Foundation Research Center, Memphis, TN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Woolard</LastName><ForeName>Stacie N</ForeName><Initials>SN</Initials><AffiliationInfo><Affiliation>1] St Jude Children's Research Hospital, Memphis, TN, USA [2] Department of Tumor Cell Biology, Memphis, TN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boyd</LastName><ForeName>Kelli L</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Department of Pathology, Vanderbilt University, Nashville, TN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hoselton</LastName><ForeName>Scott A</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>Department of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schuh</LastName><ForeName>Jane M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McCullers</LastName><ForeName>Jonathan A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>1] Department of Infectious Diseases, Memphis, TN, USA [2] St Jude Children's Research Hospital, Memphis, TN, USA [3] Department of Pediatrics, University of Tennessee Health Science Center, Children's Foundation Research Center, Memphis, TN, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN266200700005C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI066349</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>01</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Immunol Cell Biol</MedlineTA><NlmUniqueID>8706300</NlmUniqueID><ISSNLinking>0818-9641</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9008-11-1</RegistryNumber><NameOfSubstance UI="D007372">Interferons</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Immunol Cell Biol. 2014 May-Jun;92(5):389-91</RefSource><PMID Version="1">24687019</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000208" MajorTopicYN="N">Acute Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001249" MajorTopicYN="N">Asthma</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" 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