Influenza in Asthmatics: For Better or for Worse?
Identifieur interne : 000145 ( Pmc/Checkpoint ); précédent : 000144; suivant : 000146Influenza in Asthmatics: For Better or for Worse?
Auteurs : Raja Veerapandian [États-Unis] ; John D. Snyder [États-Unis] ; Amali E. Samarasinghe [États-Unis]Source :
- Frontiers in Immunology [ 1664-3224 ] ; 2018.
Abstract
Asthma and influenza are two pathologic conditions of the respiratory tract that affect millions worldwide. Influenza virus of the 2009 pandemic was highly transmissible and caused severe respiratory disease in young and middle-aged individuals. Asthma was discovered to be an underlying co-morbidity that led to hospitalizations during this influenza pandemic albeit with less severe outcomes. However, animal studies that investigated the relationship between allergic inflammation and pandemic (p)H1N1 infection, showed that while characteristics of allergic airways disease were exacerbated by this virus, governing immune responses that cause exacerbations may actually protect the host from severe outcomes associated with influenza. To better understand the relationship between asthma and severe influenza during the last pandemic, we conducted a systematic literature review of reports on hospitalized patients with asthma as a co-morbid condition during the pH1N1 season. Herein, we report that numerous other underlying conditions, such as cardiovascular, neurologic, and metabolic diseases may have been underplayed as major drivers of severe influenza during the 2009 pandemic. This review synopses, (1) asthma and influenza independently, (2) epidemiologic data surrounding asthma during the 2009 influenza pandemic, and (3) recent advances in our understanding of allergic host–pathogen interactions in the context of allergic airways disease and influenza in mouse models. Our goal is to showcase possible immunological benefits of allergic airways inflammation as countermeasures for influenza virus infections as a learning tool to discover novel pathways that can enhance our ability to hinder influenza virus replication and host pathology induced thereof.
Url:
DOI: 10.3389/fimmu.2018.01843
PubMed: 30147697
PubMed Central: 6095982
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Asthma and influenza are two pathologic conditions of the respiratory tract that affect millions worldwide. Influenza virus of the 2009 pandemic was highly transmissible and caused severe respiratory disease in young and middle-aged individuals. Asthma was discovered to be an underlying co-morbidity that led to hospitalizations during this influenza pandemic albeit with less severe outcomes. However, animal studies that investigated the relationship between allergic inflammation and pandemic (p)H1N1 infection, showed that while characteristics of allergic airways disease were exacerbated by this virus, governing immune responses that cause exacerbations may actually protect the host from severe outcomes associated with influenza. To better understand the relationship between asthma and severe influenza during the last pandemic, we conducted a systematic literature review of reports on hospitalized patients with asthma as a co-morbid condition during the pH1N1 season. Herein, we report that numerous other underlying conditions, such as cardiovascular, neurologic, and metabolic diseases may have been underplayed as major drivers of severe influenza during the 2009 pandemic. This review synopses, (1) asthma and influenza independently, (2) epidemiologic data surrounding asthma during the 2009 influenza pandemic, and (3) recent advances in our understanding of allergic host–pathogen interactions in the context of allergic airways disease and influenza in mouse models. Our goal is to showcase possible immunological benefits of allergic airways inflammation as countermeasures for influenza virus infections as a learning tool to discover novel pathways that can enhance our ability to hinder influenza virus replication and host pathology induced thereof.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Immunol</journal-id>
<journal-id journal-id-type="publisher-id">Front. Immunol.</journal-id>
<journal-title-group><journal-title>Frontiers in Immunology</journal-title>
</journal-title-group>
<issn pub-type="epub">1664-3224</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">30147697</article-id>
<article-id pub-id-type="pmc">6095982</article-id>
<article-id pub-id-type="doi">10.3389/fimmu.2018.01843</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Immunology</subject>
<subj-group><subject>Review</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Influenza in Asthmatics: For Better or for Worse?</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Veerapandian</surname>
<given-names>Raja</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<uri xlink:type="simple" xlink:href="https://frontiersin.org/people/u/534396"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Snyder</surname>
<given-names>John D.</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<uri xlink:type="simple" xlink:href="https://frontiersin.org/people/u/595933"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Samarasinghe</surname>
<given-names>Amali E.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="corresp" rid="fn001">*</xref>
<uri xlink:type="simple" xlink:href="https://frontiersin.org/people/u/379222"></uri>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup>
<institution>Department of Pediatrics, University of Tennessee Health Science Center</institution>
,<addr-line>Memphis, TN</addr-line>
,<country>United States</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Children’s Foundation Research Institute, University of Tennessee Health Science Center</institution>
,<addr-line>Memphis, TN</addr-line>
,<country>United States</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>College of Graduate Health Sciences, University of Tennessee Health Science Center</institution>
,<addr-line>Memphis, TN</addr-line>
,<country>United States</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Mats Bemark, University of Gothenburg, Sweden</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: John F. Alcorn, University of Pittsburgh, United States; Paul King, Monash University, Australia</p>
</fn>
<corresp id="fn001">*Correspondence: Amali E. Samarasinghe, <email>asamaras@uthsc.edu</email>
</corresp>
<fn fn-type="other" id="fn002"><p>Specialty section: This article was submitted to Mucosal Immunity, a section of the journal Frontiers in Immunology</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>10</day>
<month>8</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="collection"><year>2018</year>
</pub-date>
<volume>9</volume>
<elocation-id>1843</elocation-id>
<history><date date-type="received"><day>01</day>
<month>3</month>
<year>2018</year>
</date>
<date date-type="accepted"><day>26</day>
<month>7</month>
<year>2018</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2018 Veerapandian, Snyder and Samarasinghe.</copyright-statement>
<copyright-year>2018</copyright-year>
<copyright-holder>Veerapandian, Snyder and Samarasinghe</copyright-holder>
<license xlink:href="https://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p>
</license>
</permissions>
<abstract><p>Asthma and influenza are two pathologic conditions of the respiratory tract that affect millions worldwide. Influenza virus of the 2009 pandemic was highly transmissible and caused severe respiratory disease in young and middle-aged individuals. Asthma was discovered to be an underlying co-morbidity that led to hospitalizations during this influenza pandemic albeit with less severe outcomes. However, animal studies that investigated the relationship between allergic inflammation and pandemic (p)H1N1 infection, showed that while characteristics of allergic airways disease were exacerbated by this virus, governing immune responses that cause exacerbations may actually protect the host from severe outcomes associated with influenza. To better understand the relationship between asthma and severe influenza during the last pandemic, we conducted a systematic literature review of reports on hospitalized patients with asthma as a co-morbid condition during the pH1N1 season. Herein, we report that numerous other underlying conditions, such as cardiovascular, neurologic, and metabolic diseases may have been underplayed as major drivers of severe influenza during the 2009 pandemic. This review synopses, (1) asthma and influenza independently, (2) epidemiologic data surrounding asthma during the 2009 influenza pandemic, and (3) recent advances in our understanding of allergic host–pathogen interactions in the context of allergic airways disease and influenza in mouse models. Our goal is to showcase possible immunological benefits of allergic airways inflammation as countermeasures for influenza virus infections as a learning tool to discover novel pathways that can enhance our ability to hinder influenza virus replication and host pathology induced thereof.</p>
</abstract>
<kwd-group><kwd>allergic asthma</kwd>
<kwd>pandemic influenza</kwd>
<kwd>co-morbidity</kwd>
<kwd>eosinophils</kwd>
<kwd>mouse</kwd>
</kwd-group>
<funding-group><award-group><funding-source id="cn01">National Institutes of Health<named-content content-type="fundref-id">10.13039/100000002</named-content>
</funding-source>
<award-id rid="cn01">R01 AI125481</award-id>
</award-group>
</funding-group>
<counts><fig-count count="5"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="175"></ref-count>
<page-count count="15"></page-count>
<word-count count="12332"></word-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
</list>
<tree><country name="États-Unis"><noRegion><name sortKey="Veerapandian, Raja" sort="Veerapandian, Raja" uniqKey="Veerapandian R" first="Raja" last="Veerapandian">Raja Veerapandian</name>
</noRegion>
<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="Snyder, John D" sort="Snyder, John D" uniqKey="Snyder J" first="John D." last="Snyder">John D. Snyder</name>
<name sortKey="Snyder, John D" sort="Snyder, John D" uniqKey="Snyder J" first="John D." last="Snyder">John D. Snyder</name>
<name sortKey="Veerapandian, Raja" sort="Veerapandian, Raja" uniqKey="Veerapandian R" first="Raja" last="Veerapandian">Raja Veerapandian</name>
</country>
</tree>
</affiliations>
</record>
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