H2N2V1, Main, Curation, bibRecord, 001206

Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection.

Identifieur interne : 001206 ( Main/Curation ); précédent : 001205; suivant : 001207

Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection.

Source :

Journal of Infectious Diseases [ 0022-1899 ] ; 2008-08-15.

RBID : Hal:pasteur-00588953

Abstract

The mechanism for the pathogenesis of H5N1 infection in humans remains unclear. This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease. Novel findings demonstrated that COX-2, along with tumor necrosis factor alpha and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro. This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade. These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs.

Url:

https://hal-riip.archives-ouvertes.fr/pasteur-00588953

DOI: 10.1086/590499

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Le document en format XML

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</hal:affiliation>
<country>République populaire de Chine</country>
</affiliation>
</author>
<author><name sortKey="Lau, Yu Lung" sort="Lau, Yu Lung" uniqKey="Lau Y" first="Yu-Lung" last="Lau">Yu-Lung Lau</name>
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          <desc>            <address>              <addrLine>Li Ka Shing Faculty of Medicine , Hong Kong Special Administrative Region</addrLine>
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          <desc>            <address>              <addrLine>Pokfulam, Hong Kong</addrLine>
              <country key="HK"></country>
            </address>
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</tutelle>
</tutelles>
</hal:affiliation>
<country>République populaire de Chine</country>
</affiliation>
</author>
<author><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>
<affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-136023" status="VALID">          <orgName>Department of Microbiology [HKU]</orgName>
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            </address>
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<country>République populaire de Chine</country>
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<author><name sortKey="Ip, Nancy Y" sort="Ip, Nancy Y" uniqKey="Ip N" first="Nancy Y" last="Ip">Nancy Y. Ip</name>
<affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-136023" status="VALID">          <orgName>Department of Microbiology [HKU]</orgName>
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          </desc>
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<country>République populaire de Chine</country>
</affiliation>
</author>
<author><name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name>
<affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-161119" status="INCOMING">          <orgName>Department of Biochemistry</orgName>
          <desc>            <address>              <addrLine>Hong Kong Special Administrative Region</addrLine>
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            </address>
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          <desc>            <address>              <addrLine>Clear Water Bay Kowloon Hong Kong</addrLine>
              <country key="HK"></country>
            </address>
            <ref type="url">http://www.ust.hk/eng/index.htm</ref>
          </desc>
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</hal:affiliation>
<country>République populaire de Chine</country>
</affiliation>
</author>
<author><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>
<affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-136023" status="VALID">          <orgName>Department of Microbiology [HKU]</orgName>
          <desc>            <address>              <addrLine>Hong Kong Special Administrative Region, China</addrLine>
              <country key="CN"></country>
            </address>
          </desc>
          <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">10.1086/590499</idno>
<series><title level="j">Journal of Infectious Diseases</title>
<idno type="ISSN">0022-1899</idno>
<imprint><date type="datePub">2008-08-15</date>
</imprint>
</series>
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<front><div type="abstract" xml:lang="en">              <p>The mechanism for the pathogenesis of H5N1 infection in humans remains unclear. This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease. Novel findings demonstrated that COX-2, along with tumor necrosis factor alpha and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro. This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade. These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs.</p>
            </div>
</front>
</TEI>
</record>

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Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection.

Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: a mechanism for the pathogenesis of avian influenza H5N1 infection.

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