Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness▿
Identifieur interne : 000828 ( Ncbi/Merge ); précédent : 000827; suivant : 000829Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness▿
Auteurs : Frank Kirstein ; William G. C. Horsnell ; Natalie Nieuwenhuizen ; Bernhard Ryffel ; Andreas L. Lopata ; Frank BrombacherSource :
- Infection and Immunity [ 0019-9567 ] ; 2010.
Abstract
Infection with the fish parasite
Url:
DOI: 10.1128/IAI.01131-09
PubMed: 20605987
PubMed Central: 2937453
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PMC:2937453Le document en format XML
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-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness<xref ref-type="fn" rid="fn1">▿</xref>
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<author><name sortKey="Kirstein, Frank" sort="Kirstein, Frank" uniqKey="Kirstein F" first="Frank" last="Kirstein">Frank Kirstein</name>
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<author><name sortKey="Horsnell, William G C" sort="Horsnell, William G C" uniqKey="Horsnell W" first="William G. C." last="Horsnell">William G. C. Horsnell</name>
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<author><name sortKey="Nieuwenhuizen, Natalie" sort="Nieuwenhuizen, Natalie" uniqKey="Nieuwenhuizen N" first="Natalie" last="Nieuwenhuizen">Natalie Nieuwenhuizen</name>
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<author><name sortKey="Lopata, Andreas L" sort="Lopata, Andreas L" uniqKey="Lopata A" first="Andreas L." last="Lopata">Andreas L. Lopata</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>Anisakis pegreffii</italic>
-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness<xref ref-type="fn" rid="fn1">▿</xref>
</title>
<author><name sortKey="Kirstein, Frank" sort="Kirstein, Frank" uniqKey="Kirstein F" first="Frank" last="Kirstein">Frank Kirstein</name>
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<author><name sortKey="Horsnell, William G C" sort="Horsnell, William G C" uniqKey="Horsnell W" first="William G. C." last="Horsnell">William G. C. Horsnell</name>
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</affiliation>
</author>
<author><name sortKey="Nieuwenhuizen, Natalie" sort="Nieuwenhuizen, Natalie" uniqKey="Nieuwenhuizen N" first="Natalie" last="Nieuwenhuizen">Natalie Nieuwenhuizen</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
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<author><name sortKey="Ryffel, Bernhard" sort="Ryffel, Bernhard" uniqKey="Ryffel B" first="Bernhard" last="Ryffel">Bernhard Ryffel</name>
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</affiliation>
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<author><name sortKey="Lopata, Andreas L" sort="Lopata, Andreas L" uniqKey="Lopata A" first="Andreas L." last="Lopata">Andreas L. Lopata</name>
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<author><name sortKey="Brombacher, Frank" sort="Brombacher, Frank" uniqKey="Brombacher F" first="Frank" last="Brombacher">Frank Brombacher</name>
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</affiliation>
</author>
</analytic>
<series><title level="j">Infection and Immunity</title>
<idno type="ISSN">0019-9567</idno>
<idno type="eISSN">1098-5522</idno>
<imprint><date when="2010">2010</date>
</imprint>
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<front><div type="abstract" xml:lang="en"><p>Infection with the fish parasite <italic>Anisakis</italic>
following exposure to contaminated fish can lead to allergic reactions in humans. The present study examined the immunological mechanisms underlying the development of allergic airway inflammation in mice after different routes of sensitization to <italic>Anisakis</italic>
. Wild-type and interleukin-4 receptor alpha (IL-4Rα)-deficient BALB/c mice were sensitized intraperitoneally with live or heat-killed <italic>Anisakis</italic>
larvae or by intranasal administration of an <italic>Anisakis</italic>
extract and were subsequently challenged intranasally with an <italic>Anisakis</italic>
extract. Both routes of sensitization induced IL-4Rα-dependent allergic airway responses, whereas allergen-specific antibody responses developed only when mice were sensitized intraperitoneally. Intranasal sensitization induced airway hyperresponsiveness (AHR) in wild-type mice only, showing that AHR was IL-4/IL-13 dependent. Unexpectedly, infection with <italic>Anisakis</italic>
larvae induced AHR in both wild-type and IL-4Rα-deficient mice. IL-4Rα-independent AHR was mediated by gamma interferon (IFN-γ), as evidenced by the fact that <italic>in vivo</italic>
neutralization of IFN-γ abrogated AHR. Together, these results demonstrate that both infection with larvae and inhalational exposure to <italic>Anisakis</italic>
proteins are potent routes of allergic sensitization to <italic>Anisakis</italic>
, explaining food- and work-related allergies in humans. Importantly for diagnosis, allergic airway inflammation can be independent of detectable <italic>Anisakis</italic>
-specific antibodies. Moreover, depending on the route of sensitization, AHR can be induced either by IL-4/IL-13 or by IFN-γ.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Infect Immun</journal-id>
<journal-id journal-id-type="publisher-id">iai</journal-id>
<journal-title-group><journal-title>Infection and Immunity</journal-title>
</journal-title-group>
<issn pub-type="ppub">0019-9567</issn>
<issn pub-type="epub">1098-5522</issn>
<publisher><publisher-name>American Society for Microbiology (ASM)</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">20605987</article-id>
<article-id pub-id-type="pmc">2937453</article-id>
<article-id pub-id-type="publisher-id">1131-09</article-id>
<article-id pub-id-type="doi">10.1128/IAI.01131-09</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Fungal and Parasitic Infections</subject>
</subj-group>
</article-categories>
<title-group><article-title><italic>Anisakis pegreffii</italic>
-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness<xref ref-type="fn" rid="fn1">▿</xref>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Kirstein</surname>
<given-names>Frank</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Horsnell</surname>
<given-names>William G. C.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nieuwenhuizen</surname>
<given-names>Natalie</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ryffel</surname>
<given-names>Bernhard</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lopata</surname>
<given-names>Andreas L.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff1">3</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Brombacher</surname>
<given-names>Frank</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
</contrib-group>
<aff id="aff1">Division of Immunology, Institute of Infectious Disease and Molecular Medicine, Health Sciences Faculty, University of Cape Town and International Centre for Genetic Engineering and Biotechnology (ICGEB), 7925 Cape Town, South Africa,<label>1</label>
Universitè d'Orlèans, Centre National de la Recherche (CNRS), Molecular Immunology and Embryology, 45071 Orlèans, France,<label>2</label>
School of Applied Sciences, Allergy Research Group, RMIT University, Melbourne 3083, Australia<label>3</label>
</aff>
<author-notes><corresp id="cor1"><label>*</label>
Corresponding author. Mailing address: Allergy Research Group, Food Sciences, School of Applied Science, RMIT University, Melbourne 3083, Australia. Phone: 61 (0) 3 9925 6627. Fax: 61 (0) 3 9925 7110. E-mail: <email>andreas.lopata@rmit.edu.au</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>9</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="epub"><day>6</day>
<month>7</month>
<year>2010</year>
</pub-date>
<volume>78</volume>
<issue>9</issue>
<fpage>4077</fpage>
<lpage>4086</lpage>
<history><date date-type="received"><day>7</day>
<month>10</month>
<year>2009</year>
</date>
<date date-type="rev-recd"><day>15</day>
<month>12</month>
<year>2009</year>
</date>
<date date-type="accepted"><day>22</day>
<month>6</month>
<year>2010</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2010, American Society for Microbiology</copyright-statement>
<copyright-year>2010</copyright-year>
</permissions>
<self-uri xlink:title="pdf" xlink:href="zii00910004077.pdf"></self-uri>
<abstract><p>Infection with the fish parasite <italic>Anisakis</italic>
following exposure to contaminated fish can lead to allergic reactions in humans. The present study examined the immunological mechanisms underlying the development of allergic airway inflammation in mice after different routes of sensitization to <italic>Anisakis</italic>
. Wild-type and interleukin-4 receptor alpha (IL-4Rα)-deficient BALB/c mice were sensitized intraperitoneally with live or heat-killed <italic>Anisakis</italic>
larvae or by intranasal administration of an <italic>Anisakis</italic>
extract and were subsequently challenged intranasally with an <italic>Anisakis</italic>
extract. Both routes of sensitization induced IL-4Rα-dependent allergic airway responses, whereas allergen-specific antibody responses developed only when mice were sensitized intraperitoneally. Intranasal sensitization induced airway hyperresponsiveness (AHR) in wild-type mice only, showing that AHR was IL-4/IL-13 dependent. Unexpectedly, infection with <italic>Anisakis</italic>
larvae induced AHR in both wild-type and IL-4Rα-deficient mice. IL-4Rα-independent AHR was mediated by gamma interferon (IFN-γ), as evidenced by the fact that <italic>in vivo</italic>
neutralization of IFN-γ abrogated AHR. Together, these results demonstrate that both infection with larvae and inhalational exposure to <italic>Anisakis</italic>
proteins are potent routes of allergic sensitization to <italic>Anisakis</italic>
, explaining food- and work-related allergies in humans. Importantly for diagnosis, allergic airway inflammation can be independent of detectable <italic>Anisakis</italic>
-specific antibodies. Moreover, depending on the route of sensitization, AHR can be induced either by IL-4/IL-13 or by IFN-γ.</p>
</abstract>
</article-meta>
<notes><fn-group><fn><p><italic>Editor:</italic>
J. F. Urban, Jr.</p>
</fn>
</fn-group>
</notes>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Brombacher, Frank" sort="Brombacher, Frank" uniqKey="Brombacher F" first="Frank" last="Brombacher">Frank Brombacher</name>
<name sortKey="Horsnell, William G C" sort="Horsnell, William G C" uniqKey="Horsnell W" first="William G. C." last="Horsnell">William G. C. Horsnell</name>
<name sortKey="Kirstein, Frank" sort="Kirstein, Frank" uniqKey="Kirstein F" first="Frank" last="Kirstein">Frank Kirstein</name>
<name sortKey="Lopata, Andreas L" sort="Lopata, Andreas L" uniqKey="Lopata A" first="Andreas L." last="Lopata">Andreas L. Lopata</name>
<name sortKey="Nieuwenhuizen, Natalie" sort="Nieuwenhuizen, Natalie" uniqKey="Nieuwenhuizen N" first="Natalie" last="Nieuwenhuizen">Natalie Nieuwenhuizen</name>
<name sortKey="Ryffel, Bernhard" sort="Ryffel, Bernhard" uniqKey="Ryffel B" first="Bernhard" last="Ryffel">Bernhard Ryffel</name>
</noCountry>
</tree>
</affiliations>
</record>
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