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PAR1 contributes to influenza A virus pathogenicity in mice

Identifieur interne : 000442 ( Hal/Corpus ); précédent : 000441; suivant : 000443

PAR1 contributes to influenza A virus pathogenicity in mice

Auteurs : Khaled Khoufache ; Fatma Berri ; Wolfgang Nacken ; Annette B. Vogel ; Marie Delenne ; Eric Camerer ; Shaun R. Coughlin ; Peter Carmeliet ; Bruno Lina ; Guus F. Rimmelzwaan ; Oliver Planz ; Stephan Ludwig ; Beatrice Riteau

Source :

RBID : Hal:hal-02643913

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English descriptors

Abstract

Influenza causes substantial morbidity and mortality, and highly pathogenic and drug-resistant strains are likely to emerge in the future. Protease-activated receptor 1 (PAR1) is a thrombin-activated receptor that contributes to inflammatory responses at mucosal surfaces. The role of PAR1 in pathogenesis of virus infections is unknown. Here, we demonstrate that PAR1 contributed to the deleterious inflammatory response after influenza virus infection in mice. Activating PAR1 by administering the agonist TFLLR-NH2 decreased survival and increased lung inflammation after influenza infection. Importantly, both administration of a PAR1 antagonist and PAR1 deficiency protected mice from infection with influenza A viruses (IAVs). Treatment with the PAR1 agonist did not alter survival of mice deficient in plasminogen (PLG), which suggests that PLG permits and/or interacts with a PAR1 function in this model. PARE antagonists are in human trials for other indications. Our findings suggest that PAR1 antagonism might be explored as a treatment for influenza, including that caused by highly pathogenic H5N1 and oseltamivir-resistant H1N1 viruses.


Url:
DOI: 10.1172/JCI61667

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Hal:hal-02643913

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<name sortKey="Carmeliet, Peter" sort="Carmeliet, Peter" uniqKey="Carmeliet P" first="Peter" last="Carmeliet">Peter Carmeliet</name>
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<name sortKey="Lina, Bruno" sort="Lina, Bruno" uniqKey="Lina B" first="Bruno" last="Lina">Bruno Lina</name>
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<name sortKey="Rimmelzwaan, Guus F" sort="Rimmelzwaan, Guus F" uniqKey="Rimmelzwaan G" first="Guus F." last="Rimmelzwaan">Guus F. Rimmelzwaan</name>
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<orgName>Erasmus University Rotterdam</orgName>
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<name sortKey="Planz, Oliver" sort="Planz, Oliver" uniqKey="Planz O" first="Oliver" last="Planz">Oliver Planz</name>
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<name sortKey="Ludwig, Stephan" sort="Ludwig, Stephan" uniqKey="Ludwig S" first="Stephan" last="Ludwig">Stephan Ludwig</name>
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<orgName>University of Münster</orgName>
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<name sortKey="Riteau, Beatrice" sort="Riteau, Beatrice" uniqKey="Riteau B" first="Beatrice" last="Riteau">Beatrice Riteau</name>
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<addrLine>37380 Nouzilly</addrLine>
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<idno type="DOI">10.1172/JCI61667</idno>
<series>
<title level="j">Journal of Clinical Investigation</title>
<idno type="ISSN">0021-9738</idno>
<imprint>
<date type="datePub">2013</date>
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<keywords scheme="mix" xml:lang="en">
<term>ANTAGONIST VORAPAXAR</term>
<term>DEPENDENT PATHWAY</term>
<term>IN-VIVO</term>
<term>LUNG INJURY</term>
<term>PROTEASE-ACTIVATED RECEPTORS</term>
<term>THROMBIN</term>
</keywords>
<keywords scheme="mix" xml:lang="fr">
<term>INFECTION</term>
<term>INFLAMMATION</term>
<term>PANDEMIC INFLUENZA</term>
<term>PLASMINOGEN</term>
</keywords>
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<front>
<div type="abstract" xml:lang="en">
<p>Influenza causes substantial morbidity and mortality, and highly pathogenic and drug-resistant strains are likely to emerge in the future. Protease-activated receptor 1 (PAR1) is a thrombin-activated receptor that contributes to inflammatory responses at mucosal surfaces. The role of PAR1 in pathogenesis of virus infections is unknown. Here, we demonstrate that PAR1 contributed to the deleterious inflammatory response after influenza virus infection in mice. Activating PAR1 by administering the agonist TFLLR-NH2 decreased survival and increased lung inflammation after influenza infection. Importantly, both administration of a PAR1 antagonist and PAR1 deficiency protected mice from infection with influenza A viruses (IAVs). Treatment with the PAR1 agonist did not alter survival of mice deficient in plasminogen (PLG), which suggests that PLG permits and/or interacts with a PAR1 function in this model. PARE antagonists are in human trials for other indications. Our findings suggest that PAR1 antagonism might be explored as a treatment for influenza, including that caused by highly pathogenic H5N1 and oseltamivir-resistant H1N1 viruses.</p>
</div>
</front>
</TEI>
<hal api="V3">
<titleStmt>
<title xml:lang="en">PAR1 contributes to influenza A virus pathogenicity in mice</title>
<author role="aut">
<persName>
<forename type="first">Khaled</forename>
<surname>Khoufache</surname>
</persName>
<email type="md5">547e112479f45f8da81c026caad07355</email>
<email type="domain">yahoo.fr</email>
<idno type="halauthorid">197742</idno>
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</author>
<author role="aut">
<persName>
<forename type="first">Fatma</forename>
<surname>Berri</surname>
</persName>
<idno type="halauthorid">1003479</idno>
<affiliation ref="#struct-508819"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Wolfgang</forename>
<surname>Nacken</surname>
</persName>
<idno type="halauthorid">548374</idno>
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</author>
<author role="aut">
<persName>
<forename type="first">Annette B.</forename>
<surname>Vogel</surname>
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</author>
<author role="aut">
<persName>
<forename type="first">Marie</forename>
<surname>Delenne</surname>
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<idno type="halauthorid">11877132</idno>
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<author role="aut">
<persName>
<forename type="first">Eric</forename>
<surname>Camerer</surname>
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<author role="aut">
<persName>
<forename type="first">Shaun R.</forename>
<surname>Coughlin</surname>
</persName>
<idno type="halauthorid">11726681</idno>
<affiliation ref="#struct-190541"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Peter</forename>
<surname>Carmeliet</surname>
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<idno type="halauthorid">193904</idno>
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<author role="aut">
<persName>
<forename type="first">Bruno</forename>
<surname>Lina</surname>
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<idno type="halauthorid">400981</idno>
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<author role="aut">
<persName>
<forename type="first">Guus F.</forename>
<surname>Rimmelzwaan</surname>
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<idno type="halauthorid">11877133</idno>
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<persName>
<forename type="first">Oliver</forename>
<surname>Planz</surname>
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<idno type="halauthorid">11877134</idno>
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</author>
<author role="aut">
<persName>
<forename type="first">Stephan</forename>
<surname>Ludwig</surname>
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<idno type="halauthorid">11870369</idno>
<affiliation ref="#struct-425052"></affiliation>
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<author role="aut">
<persName>
<forename type="first">Beatrice</forename>
<surname>Riteau</surname>
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<email type="domain">univ-lyon1.fr</email>
<idno type="halauthorid">1208506</idno>
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<forename>Migration</forename>
<surname>ProdInra</surname>
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<email type="md5">9e5ed7d56b52b3d4383123b1ffb42236</email>
<email type="domain">inrae.fr</email>
</editor>
<funder>Agence Nationale de la Recherche (ANR); Inserm Avenir; Marie Curie actions; Long-term structural funding-Methusalem by the Flemish government</funder>
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<edition n="v1" type="current">
<date type="whenSubmitted">2020-05-28 20:54:51</date>
<date type="whenModified">2020-05-30 03:42:50</date>
<date type="whenReleased">2020-05-28 20:54:51</date>
<date type="whenProduced">2013</date>
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<idno type="halId">hal-02643913</idno>
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<idno type="halRefHtml">Journal of Clinical Investigation, American Society for Clinical Investigation, 2013, 123 (1), pp.206 - 214. ⟨10.1172/JCI61667⟩</idno>
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<idno type="stamp" n="INRAE">Institut National de Recherche en Agriculture, Alimentation et Environnement</idno>
<idno type="stamp" n="INRA">INRA - Institut national de la recherche agronomique</idno>
<idno type="stamp" n="APHP" corresp="INSERM">AP-HP</idno>
<idno type="stamp" n="UNIV-LYON1">Université Claude Bernard - Lyon I</idno>
<idno type="stamp" n="CHU-UNIV-PARIS5">Les centres hospitaliers de Paris Descartes</idno>
<idno type="stamp" n="UNIV-TOURS">Université François Rabelais</idno>
<idno type="stamp" n="UDL">UDL</idno>
<idno type="stamp" n="UNIV-LYON">Université de Lyon</idno>
<idno type="stamp" n="UNIV-PARIS5" corresp="UNIV-PARIS">Université Paris Descartes (Paris 5)</idno>
<idno type="stamp" n="UP-SANTE">Université de Paris - Faculté de Santé</idno>
<idno type="stamp" n="INSERM">INSERM - Institut national de la santé et de la recherche médicale</idno>
<idno type="stamp" n="USPC">Université Sorbonne Paris Cité</idno>
<idno type="stamp" n="UNIV-PARIS">Université de Paris</idno>
</seriesStmt>
<notesStmt>
<note type="popular" n="0">No</note>
<note type="peer" n="1">Yes</note>
</notesStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en">PAR1 contributes to influenza A virus pathogenicity in mice</title>
<author role="aut">
<persName>
<forename type="first">Khaled</forename>
<surname>Khoufache</surname>
</persName>
<email type="md5">547e112479f45f8da81c026caad07355</email>
<email type="domain">yahoo.fr</email>
<idno type="halauthorid">197742</idno>
<affiliation ref="#struct-211885"></affiliation>
<affiliation ref="#struct-508819"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Fatma</forename>
<surname>Berri</surname>
</persName>
<idno type="halauthorid">1003479</idno>
<affiliation ref="#struct-508819"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Wolfgang</forename>
<surname>Nacken</surname>
</persName>
<idno type="halauthorid">548374</idno>
<affiliation ref="#struct-425052"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Annette B.</forename>
<surname>Vogel</surname>
</persName>
<idno type="halauthorid">11877131</idno>
<affiliation ref="#struct-322700"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Marie</forename>
<surname>Delenne</surname>
</persName>
<idno type="halauthorid">11877132</idno>
<affiliation ref="#struct-508819"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Eric</forename>
<surname>Camerer</surname>
</persName>
<idno type="halauthorid">1557508</idno>
<affiliation ref="#struct-81503"></affiliation>
<affiliation ref="#struct-301664"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Shaun R.</forename>
<surname>Coughlin</surname>
</persName>
<idno type="halauthorid">11726681</idno>
<affiliation ref="#struct-190541"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Peter</forename>
<surname>Carmeliet</surname>
</persName>
<idno type="halauthorid">193904</idno>
<affiliation ref="#struct-357456"></affiliation>
<affiliation ref="#struct-92863"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Bruno</forename>
<surname>Lina</surname>
</persName>
<idno type="halauthorid">400981</idno>
<affiliation ref="#struct-508819"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Guus F.</forename>
<surname>Rimmelzwaan</surname>
</persName>
<idno type="halauthorid">11877133</idno>
<affiliation ref="#struct-485122"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Oliver</forename>
<surname>Planz</surname>
</persName>
<idno type="halauthorid">11877134</idno>
<affiliation ref="#struct-322700"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Stephan</forename>
<surname>Ludwig</surname>
</persName>
<idno type="halauthorid">11870369</idno>
<affiliation ref="#struct-425052"></affiliation>
</author>
<author role="aut">
<persName>
<forename type="first">Beatrice</forename>
<surname>Riteau</surname>
</persName>
<email type="md5">3e2374cca8aec85f239e07ef3201be28</email>
<email type="domain">univ-lyon1.fr</email>
<idno type="halauthorid">1208506</idno>
<affiliation ref="#struct-211885"></affiliation>
<affiliation ref="#struct-194495"></affiliation>
</author>
</analytic>
<monogr>
<idno type="halJournalId" status="VALID">1386</idno>
<idno type="issn">0021-9738</idno>
<title level="j">Journal of Clinical Investigation</title>
<imprint>
<publisher>American Society for Clinical Investigation</publisher>
<biblScope unit="volume">123</biblScope>
<biblScope unit="issue">1</biblScope>
<biblScope unit="pp">206 - 214</biblScope>
<date type="datePub">2013</date>
</imprint>
</monogr>
<idno type="doi">10.1172/JCI61667</idno>
<idno type="prodinra">211606</idno>
<idno type="wos">000313598500026</idno>
</biblStruct>
</sourceDesc>
<profileDesc>
<langUsage>
<language ident="en">English</language>
</langUsage>
<textClass>
<keywords scheme="author">
<term xml:lang="en">PROTEASE-ACTIVATED RECEPTORS</term>
<term xml:lang="en">ANTAGONIST VORAPAXAR</term>
<term xml:lang="en">DEPENDENT PATHWAY</term>
<term xml:lang="en">LUNG INJURY</term>
<term xml:lang="en">IN-VIVO</term>
<term xml:lang="en">THROMBIN</term>
<term xml:lang="fr">PANDEMIC INFLUENZA</term>
<term xml:lang="fr">PLASMINOGEN</term>
<term xml:lang="fr">INFECTION</term>
<term xml:lang="fr">INFLAMMATION</term>
</keywords>
<classCode scheme="halDomain" n="sdv">Life Sciences [q-bio]</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en">
<p>Influenza causes substantial morbidity and mortality, and highly pathogenic and drug-resistant strains are likely to emerge in the future. Protease-activated receptor 1 (PAR1) is a thrombin-activated receptor that contributes to inflammatory responses at mucosal surfaces. The role of PAR1 in pathogenesis of virus infections is unknown. Here, we demonstrate that PAR1 contributed to the deleterious inflammatory response after influenza virus infection in mice. Activating PAR1 by administering the agonist TFLLR-NH2 decreased survival and increased lung inflammation after influenza infection. Importantly, both administration of a PAR1 antagonist and PAR1 deficiency protected mice from infection with influenza A viruses (IAVs). Treatment with the PAR1 agonist did not alter survival of mice deficient in plasminogen (PLG), which suggests that PLG permits and/or interacts with a PAR1 function in this model. PARE antagonists are in human trials for other indications. Our findings suggest that PAR1 antagonism might be explored as a treatment for influenza, including that caused by highly pathogenic H5N1 and oseltamivir-resistant H1N1 viruses.</p>
</abstract>
</profileDesc>
</hal>
</record>

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