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Innate immune response to a H3N2 subtype swine influenza virus in newborn porcine trachea cells, alveolar macrophages, and precision-cut lung slices

Identifieur interne : 000171 ( Hal/Corpus ); précédent : 000170; suivant : 000172

Innate immune response to a H3N2 subtype swine influenza virus in newborn porcine trachea cells, alveolar macrophages, and precision-cut lung slices

Auteurs : Mario Delgado-Ortega ; Sandrina Pereira Melo ; Darsaniya Punyadarsaniya ; Christelle Rame ; Michel Olivier ; Denis Soubieux ; Daniel Marc ; Gaëlle Simon ; Georg Herrler ; El Mostafa Berri ; Joëlle Dupont ; François Meurens

Source :

RBID : Hal:hal-01129833

Abstract

Viral respiratory diseases remain of major importance in swine breeding units. Swine influenza virus (SIV) is one of the main known contributors to infectious respiratory diseases. The innate immune response to swine influenza viruses has been assessed in many previous studies. However most of these studies were carried out in a single-cell population or directly in the live animal, in all its complexity. In the current study we report the use of a trachea epithelial cell line (newborn pig trachea cells - NPTr) in comparison with alveolar macrophages and lung slices for the characterization of innate immune response to an infection by a European SIV of the H3N2 subtype. The expression pattern of transcripts involved in the recognition of the virus, interferon type I and III responses, and the host-response regulation were assessed by quantitative PCR in response to infection. Some significant differences were observed between the three systems, notably in the expression of type III interferon mRNA. Then, results show a clear induction of JAK/STAT and MAPK signaling pathways in infected NPTr cells. Conversely, PI3K/Akt signaling pathways was not activated. The inhibition of the JAK/STAT pathway clearly reduced interferon type I and III responses and the induction of SOCS1 at the transcript level in infected NPTr cells. Similarly, the inhibition of MAPK pathway reduced viral replication and interferon response. All together, these results contribute to an increased understanding of the innate immune response to H3N2 SIV and may help identify strategies to effectively control SIV infection.


Url:
DOI: 10.1186/1297-9716-45-42

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Hal:hal-01129833

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<name sortKey="Meurens, Francois" sort="Meurens, Francois" uniqKey="Meurens F" first="François" last="Meurens">François Meurens</name>
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<orgName>Vaccine and Infectious Disease Organization-InterVac</orgName>
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<idno type="DOI">10.1186/1297-9716-45-42</idno>
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<title level="j">Veterinary Research</title>
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<p>Viral respiratory diseases remain of major importance in swine breeding units. Swine influenza virus (SIV) is one of the main known contributors to infectious respiratory diseases. The innate immune response to swine influenza viruses has been assessed in many previous studies. However most of these studies were carried out in a single-cell population or directly in the live animal, in all its complexity. In the current study we report the use of a trachea epithelial cell line (newborn pig trachea cells - NPTr) in comparison with alveolar macrophages and lung slices for the characterization of innate immune response to an infection by a European SIV of the H3N2 subtype. The expression pattern of transcripts involved in the recognition of the virus, interferon type I and III responses, and the host-response regulation were assessed by quantitative PCR in response to infection. Some significant differences were observed between the three systems, notably in the expression of type III interferon mRNA. Then, results show a clear induction of JAK/STAT and MAPK signaling pathways in infected NPTr cells. Conversely, PI3K/Akt signaling pathways was not activated. The inhibition of the JAK/STAT pathway clearly reduced interferon type I and III responses and the induction of SOCS1 at the transcript level in infected NPTr cells. Similarly, the inhibition of MAPK pathway reduced viral replication and interferon response. All together, these results contribute to an increased understanding of the innate immune response to H3N2 SIV and may help identify strategies to effectively control SIV infection.</p>
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<title xml:lang="en">Innate immune response to a H3N2 subtype swine influenza virus in newborn porcine trachea cells, alveolar macrophages, and precision-cut lung slices</title>
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<forename type="first">Mario</forename>
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<forename type="first">Sandrina</forename>
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<forename type="first">Darsaniya</forename>
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<forename type="first">Gaëlle</forename>
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<funder>Institut National de la Recherche Agronomique (INRA), Conseil Regional du Centre (France), Natural Science and Engineering Research Council of Canada (NSERC) 435887-2013, German FluResearchNet, a nationwide research network on zoonotic influenza - Ministry of Education and Research</funder>
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<idno type="stamp" n="ANSES">Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail</idno>
<idno type="stamp" n="INRA">INRA - Institut national de la recherche agronomique</idno>
<idno type="stamp" n="GIP-BE">GIP Bretagne Environnement</idno>
<idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno>
<idno type="stamp" n="UNIV-TOURS">Université François Rabelais</idno>
<idno type="stamp" n="INRAE">Institut National de Recherche en Agriculture, Alimentation et Environnement</idno>
</seriesStmt>
<notesStmt>
<note type="audience" n="1">Not set</note>
<note type="popular" n="0">No</note>
<note type="peer" n="1">Yes</note>
</notesStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en">Innate immune response to a H3N2 subtype swine influenza virus in newborn porcine trachea cells, alveolar macrophages, and precision-cut lung slices</title>
<author role="aut">
<persName>
<forename type="first">Mario</forename>
<surname>Delgado-Ortega</surname>
</persName>
<email type="md5">b00806bff75ed4f0d74cbea4a264f3a9</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1141508</idno>
<affiliation ref="#struct-41761"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Sandrina</forename>
<surname>Pereira Melo</surname>
</persName>
<email type="md5">cf12e447b24d4bd2bb0ad65c5c349cd9</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1141511</idno>
<affiliation ref="#struct-41761"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Darsaniya</forename>
<surname>Punyadarsaniya</surname>
</persName>
<idno type="halauthorid">1142137</idno>
<affiliation ref="#struct-415483"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Christelle</forename>
<surname>Rame</surname>
</persName>
<email type="md5">9c3f2b2e1fad77d72a66c65b5cb5bed8</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1141122</idno>
<affiliation ref="#struct-199335"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Michel</forename>
<surname>Olivier</surname>
</persName>
<email type="md5">1a58538a810497d6bd97cef2ce8f0c5b</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1142138</idno>
<affiliation ref="#struct-41761"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Denis</forename>
<surname>Soubieux</surname>
</persName>
<email type="md5">91712bdc554c260c84961eddf418d8e5</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1140223</idno>
<affiliation ref="#struct-41761"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Daniel</forename>
<surname>Marc</surname>
</persName>
<email type="md5">4a4b83de0cd63bdeb6f8f08dc8a407df</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1140229</idno>
<affiliation ref="#struct-41761"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Gaëlle</forename>
<surname>Simon</surname>
</persName>
<idno type="halauthorid">689844</idno>
<affiliation ref="#struct-415484"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Georg</forename>
<surname>Herrler</surname>
</persName>
<idno type="halauthorid">726300</idno>
<affiliation ref="#struct-415485"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">El Mostafa</forename>
<surname>Berri</surname>
</persName>
<email type="md5">59cc8ee96f18ac42cbbd8b3c283e04c8</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1142139</idno>
<affiliation ref="#struct-41761"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Joëlle</forename>
<surname>Dupont</surname>
</persName>
<email type="md5">e9cfc2e060b28a935d7975354139c830</email>
<email type="domain">tours.inra.fr</email>
<idno type="halauthorid">1049856</idno>
<affiliation ref="#struct-199335"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">François</forename>
<surname>Meurens</surname>
</persName>
<idno type="halauthorid">397425</idno>
<affiliation ref="#struct-415486"></affiliation>
</author>
</analytic>
<monogr>
<idno type="halJournalId" status="VALID">19840</idno>
<idno type="issn">0928-4249</idno>
<idno type="eissn">1297-9716</idno>
<title level="j">Veterinary Research</title>
<imprint>
<publisher>BioMed Central</publisher>
<biblScope unit="volume">45</biblScope>
<biblScope unit="issue">1</biblScope>
<biblScope unit="pp">1-18</biblScope>
<date type="datePub">2014</date>
</imprint>
</monogr>
<idno type="doi">10.1186/1297-9716-45-42</idno>
<idno type="prodinra">259219</idno>
<idno type="pubmed">24712747</idno>
</biblStruct>
</sourceDesc>
<profileDesc>
<langUsage>
<language ident="en">English</language>
</langUsage>
<textClass>
<classCode scheme="halDomain" n="sdv.ot">Life Sciences [q-bio]/Other [q-bio.OT]</classCode>
<classCode scheme="halDomain" n="sdv.imm">Life Sciences [q-bio]/Immunology</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en">
<p>Viral respiratory diseases remain of major importance in swine breeding units. Swine influenza virus (SIV) is one of the main known contributors to infectious respiratory diseases. The innate immune response to swine influenza viruses has been assessed in many previous studies. However most of these studies were carried out in a single-cell population or directly in the live animal, in all its complexity. In the current study we report the use of a trachea epithelial cell line (newborn pig trachea cells - NPTr) in comparison with alveolar macrophages and lung slices for the characterization of innate immune response to an infection by a European SIV of the H3N2 subtype. The expression pattern of transcripts involved in the recognition of the virus, interferon type I and III responses, and the host-response regulation were assessed by quantitative PCR in response to infection. Some significant differences were observed between the three systems, notably in the expression of type III interferon mRNA. Then, results show a clear induction of JAK/STAT and MAPK signaling pathways in infected NPTr cells. Conversely, PI3K/Akt signaling pathways was not activated. The inhibition of the JAK/STAT pathway clearly reduced interferon type I and III responses and the induction of SOCS1 at the transcript level in infected NPTr cells. Similarly, the inhibition of MAPK pathway reduced viral replication and interferon response. All together, these results contribute to an increased understanding of the innate immune response to H3N2 SIV and may help identify strategies to effectively control SIV infection.</p>
</abstract>
</profileDesc>
</hal>
</record>

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