H2N2V1, Main, Exploration, bibRecord, 001014

Induction of proinflammatory cytokines in primary human macrophages by influenza A virus (H5N1) is selectively regulated by IFN regulatory factor 3 and p38 MAPK.

Identifieur interne : 001014 ( Main/Exploration ); précédent : 001013; suivant : 001015

Induction of proinflammatory cytokines in primary human macrophages by influenza A virus (H5N1) is selectively regulated by IFN regulatory factor 3 and p38 MAPK.

Auteurs : Kenrie P Y. Hui [République populaire de Chine] ; Suki M Y. Lee [République populaire de Chine] ; Chung-Yan Cheung [République populaire de Chine] ; Iris H Y. Ng [République populaire de Chine] ; Leo L M. Poon [République populaire de Chine] ; Yi Guan [République populaire de Chine] ; Nancy Y Y. Ip [République populaire de Chine] ; Allan S Y. Lau [République populaire de Chine] ; J S Malik Peiris [République populaire de Chine]

Source :

Journal of Immunology [ 0022-1767 ] ; 2009-01-15.

RBID : Hal:pasteur-00588949

Abstract

The hyperinduction of proinflammatory cytokines and chemokines such as TNF-alpha, IFN-beta, and CCL2/MCP-1 in primary human macrophages and respiratory epithelial cells by the highly pathogenic avian influenza H5N1 is believed to contribute to the unusual severity of human H5N1 disease. Here we show that TNF-alpha, IFN-beta, and IFN-lambda1 are the key mediators directly induced by the H5N1 virus in primary human macrophages. In comparison with human influenza (H1N1), the H5N1 virus more strongly activated IFN regulatory factor 3 (IRF3). IRF3 knockdown and p38 kinase inhibition separately and in combination led to a substantial reduction of IFN-beta, IFN-lambda1, and MCP-1 but only to a partial reduction of TNF-alpha. IRF3 translocation was independent of p38 kinase activity, indicating that IRF3 and p38 kinase are distinct pathways leading to cytokine production by H5N1 virus. We conclude that IRF3 and p38 kinase separately and predominantly contribute to H5N1-mediated induction of IFN-beta, IFN-lambda1, and MCP-1 but only partly control TNF-alpha induction. A more precise identification of the differences in the regulation of TNF-alpha and IFN-beta could provide novel targets for the design of therapeutic strategies for severe human H5N1 influenza and also for treating other causes of acute respiratory distress syndrome.

Url:

https://hal-riip.archives-ouvertes.fr/pasteur-00588949

DOI: 10.4049/jimmunol.182.2.1088

Affiliations:

République populaire de Chine

Links toward previous steps (curation, corpus...)

to stream Hal, to step Corpus: 000155
to stream Hal, to step Curation: 000155
to stream Hal, to step Checkpoint: 000299
to stream Main, to step Merge: 001022
to stream Main, to step Curation: 001014

Le document en format XML

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          <listRelation>            <relation active="#struct-93487" type="direct"></relation>
          </listRelation>
        <tutelles><tutelle active="#struct-93487" type="direct"><org type="institution" xml:id="struct-93487" status="VALID">          <orgName>The University of Hong Kong</orgName>
          <orgName type="acronym">HKU</orgName>
          <desc>            <address>              <addrLine>Pokfulam, Hong Kong</addrLine>
              <country key="HK"></country>
            </address>
            <ref type="url">http://www.hku.hk/</ref>
          </desc>
        </org>
</tutelle>
</tutelles>
</hal:affiliation>
<country>République populaire de Chine</country>
</affiliation>
</author>
</analytic>
<idno type="DOI">10.4049/jimmunol.182.2.1088</idno>
<series><title level="j">Journal of Immunology</title>
<idno type="ISSN">0022-1767</idno>
<imprint><date type="datePub">2009-01-15</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">              <p>The hyperinduction of proinflammatory cytokines and chemokines such as TNF-alpha, IFN-beta, and CCL2/MCP-1 in primary human macrophages and respiratory epithelial cells by the highly pathogenic avian influenza H5N1 is believed to contribute to the unusual severity of human H5N1 disease. Here we show that TNF-alpha, IFN-beta, and IFN-lambda1 are the key mediators directly induced by the H5N1 virus in primary human macrophages. In comparison with human influenza (H1N1), the H5N1 virus more strongly activated IFN regulatory factor 3 (IRF3). IRF3 knockdown and p38 kinase inhibition separately and in combination led to a substantial reduction of IFN-beta, IFN-lambda1, and MCP-1 but only to a partial reduction of TNF-alpha. IRF3 translocation was independent of p38 kinase activity, indicating that IRF3 and p38 kinase are distinct pathways leading to cytokine production by H5N1 virus. We conclude that IRF3 and p38 kinase separately and predominantly contribute to H5N1-mediated induction of IFN-beta, IFN-lambda1, and MCP-1 but only partly control TNF-alpha induction. A more precise identification of the differences in the regulation of TNF-alpha and IFN-beta could provide novel targets for the design of therapeutic strategies for severe human H5N1 influenza and also for treating other causes of acute respiratory distress syndrome.</p>
            </div>
</front>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Hui, Kenrie P Y" sort="Hui, Kenrie P Y" uniqKey="Hui K" first="Kenrie P Y" last="Hui">Kenrie P Y. Hui</name>
</noRegion>
<name sortKey="Cheung, Chung Yan" sort="Cheung, Chung Yan" uniqKey="Cheung C" first="Chung-Yan" last="Cheung">Chung-Yan Cheung</name>
<name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name>
<name sortKey="Ip, Nancy Y Y" sort="Ip, Nancy Y Y" uniqKey="Ip N" first="Nancy Y Y" last="Ip">Nancy Y Y. Ip</name>
<name sortKey="Lau, Allan S Y" sort="Lau, Allan S Y" uniqKey="Lau A" first="Allan S Y" last="Lau">Allan S Y. Lau</name>
<name sortKey="Lee, Suki M Y" sort="Lee, Suki M Y" uniqKey="Lee S" first="Suki M Y" last="Lee">Suki M Y. Lee</name>
<name sortKey="Ng, Iris H Y" sort="Ng, Iris H Y" uniqKey="Ng I" first="Iris H Y" last="Ng">Iris H Y. Ng</name>
<name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name>
<name sortKey="Poon, Leo L M" sort="Poon, Leo L M" uniqKey="Poon L" first="Leo L M" last="Poon">Leo L M. Poon</name>
</country>
</tree>
</affiliations>
</record>

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Induction of proinflammatory cytokines in primary human macrophages by influenza A virus (H5N1) is selectively regulated by IFN regulatory factor 3 and p38 MAPK.

Induction of proinflammatory cytokines in primary human macrophages by influenza A virus (H5N1) is selectively regulated by IFN regulatory factor 3 and p38 MAPK.

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