H3N2 Influenza A Virus Replicates in Immortalized Human First Trimester Trophoblast Cell Lines and Induces Their Rapid Apoptosis
Identifieur interne : 000406 ( Ncbi/Merge ); précédent : 000405; suivant : 000407H3N2 Influenza A Virus Replicates in Immortalized Human First Trimester Trophoblast Cell Lines and Induces Their Rapid Apoptosis
Auteurs : Quang Duy Trinh [Japon] ; Yasuyuki Izumi [Japon] ; Shihoko Komine-Aizawa [Japon] ; Toshikatsu Shibata [Japon] ; Yoshitaka Shimotai [Japon] ; Kazumichi Kuroda [Japon] ; Masashi Mizuguchi [Japon] ; Hiroshi Ushijima [Japon] ; Gil Mor [États-Unis] ; Satoshi Hayakawa [Japon]Source :
- American journal of reproductive immunology (New York, N.Y. : 1989) [ 1046-7408 ] ; 2009.
Abstract
Epidemiological data suggested that pandemic influenza increased the risks of spontaneous abortion and premature labor, while seasonal influenza also increased the risk of schizophrenia in adolescence. However, their pathogenesis is so far unknown.
The first trimester trophoblast cell lines, namely, Swan71 and HTR8 cells were challenged with A/Udorn/72 influenza virus (H3N2). At indicated time points, cells were examined for expression of influenza proteins. Viral replication in culture media, apoptosis and the expression of human leukocyte antigen (HLA)-G were also examined.
Intracellular localization of viral proteins was observed. Twenty-four hours after inoculation, virus was detected in culture media while most cells fell into apoptosis. During apoptosis, expression of HLA-G was unchanged.
We revealed replication of low pathogenic influenza virus in the first trimester trophoblast cell lines. Placental damages are likely to be induced by direct cytopathic effects of influenza virus and subsequent apoptosis rather than down regulation of HLA-G expression and subsequent rejection by maternal immune system.
Url:
DOI: 10.1111/j.1600-0897.2009.00723.x
PubMed: 19694639
PubMed Central: 3025808
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<wicri:regionArea> Department of Obstetrics, Gynecology and Reproductive Sciences, Reproductive Immunology Unit, Yale University School of Medicine, New Haven, CT</wicri:regionArea>
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<author><name sortKey="Hayakawa, Satoshi" sort="Hayakawa, Satoshi" uniqKey="Hayakawa S" first="Satoshi" last="Hayakawa">Satoshi Hayakawa</name>
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<author><name sortKey="Kuroda, Kazumichi" sort="Kuroda, Kazumichi" uniqKey="Kuroda K" first="Kazumichi" last="Kuroda">Kazumichi Kuroda</name>
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<author><name sortKey="Ushijima, Hiroshi" sort="Ushijima, Hiroshi" uniqKey="Ushijima H" first="Hiroshi" last="Ushijima">Hiroshi Ushijima</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea> Department of Obstetrics, Gynecology and Reproductive Sciences, Reproductive Immunology Unit, Yale University School of Medicine, New Haven, CT</wicri:regionArea>
<placeName><region type="state">Connecticut</region>
</placeName>
</affiliation>
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<author><name sortKey="Hayakawa, Satoshi" sort="Hayakawa, Satoshi" uniqKey="Hayakawa S" first="Satoshi" last="Hayakawa">Satoshi Hayakawa</name>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Problem</title>
<p id="P1">Epidemiological data suggested that pandemic influenza increased the risks of spontaneous abortion and premature labor, while seasonal influenza also increased the risk of schizophrenia in adolescence. However, their pathogenesis is so far unknown.</p>
</sec>
<sec id="S2"><title>Method of study</title>
<p id="P2">The first trimester trophoblast cell lines, namely, Swan71 and HTR8 cells were challenged with A/Udorn/72 influenza virus (H3N2). At indicated time points, cells were examined for expression of influenza proteins. Viral replication in culture media, apoptosis and the expression of human leukocyte antigen (HLA)-G were also examined.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">Intracellular localization of viral proteins was observed. Twenty-four hours after inoculation, virus was detected in culture media while most cells fell into apoptosis. During apoptosis, expression of HLA-G was unchanged.</p>
</sec>
<sec id="S4"><title>Conclusion</title>
<p id="P4">We revealed replication of low pathogenic influenza virus in the first trimester trophoblast cell lines. Placental damages are likely to be induced by direct cytopathic effects of influenza virus and subsequent apoptosis rather than down regulation of HLA-G expression and subsequent rejection by maternal immune system.</p>
</sec>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8912860</journal-id>
<journal-id journal-id-type="pubmed-jr-id">1403</journal-id>
<journal-id journal-id-type="nlm-ta">Am J Reprod Immunol</journal-id>
<journal-title>American journal of reproductive immunology (New York, N.Y. : 1989)</journal-title>
<issn pub-type="ppub">1046-7408</issn>
<issn pub-type="epub">1600-0897</issn>
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<article-id pub-id-type="pmc">3025808</article-id>
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<article-id pub-id-type="manuscript">NIHMS263792</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>H3N2 Influenza A Virus Replicates in Immortalized Human First Trimester Trophoblast Cell Lines and Induces Their Rapid Apoptosis</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Trinh</surname>
<given-names>Quang Duy</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
<xref rid="A2" ref-type="aff">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Izumi</surname>
<given-names>Yasuyuki</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Komine-Aizawa</surname>
<given-names>Shihoko</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Shibata</surname>
<given-names>Toshikatsu</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Shimotai</surname>
<given-names>Yoshitaka</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kuroda</surname>
<given-names>Kazumichi</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Mizuguchi</surname>
<given-names>Masashi</given-names>
</name>
<xref rid="A2" ref-type="aff">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ushijima</surname>
<given-names>Hiroshi</given-names>
</name>
<xref rid="A3" ref-type="aff">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Mor</surname>
<given-names>Gil</given-names>
</name>
<xref rid="A4" ref-type="aff">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hayakawa</surname>
<given-names>Satoshi</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Division of Microbiology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Japan</aff>
<aff id="A2"><label>2</label>
Department of Developmental Medical Sciences, Institute of International Health, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan</aff>
<aff id="A3"><label>3</label>
Aino Health Science Center, Aino University, Tokyo, Japan</aff>
<aff id="A4"><label>4</label>
Department of Obstetrics, Gynecology and Reproductive Sciences, Reproductive Immunology Unit, Yale University School of Medicine, New Haven, CT, USA</aff>
<author-notes><corresp id="FN1">Correspondence: Satoshi Hayakawa, Nihon University School of Medicine, 30-1 Ohyaguchi Kamimachi, Itabashiku, Tokyo 173-8610, Japan. <email>satoshih@med.nihon-u.ac.jp</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>12</day>
<month>1</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="ppub"><month>9</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>24</day>
<month>1</month>
<year>2011</year>
</pub-date>
<volume>62</volume>
<issue>3</issue>
<fpage>139</fpage>
<lpage>146</lpage>
<abstract><sec id="S1"><title>Problem</title>
<p id="P1">Epidemiological data suggested that pandemic influenza increased the risks of spontaneous abortion and premature labor, while seasonal influenza also increased the risk of schizophrenia in adolescence. However, their pathogenesis is so far unknown.</p>
</sec>
<sec id="S2"><title>Method of study</title>
<p id="P2">The first trimester trophoblast cell lines, namely, Swan71 and HTR8 cells were challenged with A/Udorn/72 influenza virus (H3N2). At indicated time points, cells were examined for expression of influenza proteins. Viral replication in culture media, apoptosis and the expression of human leukocyte antigen (HLA)-G were also examined.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">Intracellular localization of viral proteins was observed. Twenty-four hours after inoculation, virus was detected in culture media while most cells fell into apoptosis. During apoptosis, expression of HLA-G was unchanged.</p>
</sec>
<sec id="S4"><title>Conclusion</title>
<p id="P4">We revealed replication of low pathogenic influenza virus in the first trimester trophoblast cell lines. Placental damages are likely to be induced by direct cytopathic effects of influenza virus and subsequent apoptosis rather than down regulation of HLA-G expression and subsequent rejection by maternal immune system.</p>
</sec>
</abstract>
<kwd-group><kwd>Apoptosis</kwd>
<kwd>first trimester trophoblast</kwd>
<kwd>influenza A virus</kwd>
</kwd-group>
<contract-num rid="HD1">P01 HD054713-03
||HD</contract-num>
<contract-sponsor id="HD1">National Institute of Child Health & Human Development : NICHD</contract-sponsor>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Japon</li>
<li>États-Unis</li>
</country>
<region><li>Connecticut</li>
<li>Région de Kantō</li>
</region>
<settlement><li>Tokyo</li>
</settlement>
<orgName><li>Université de Tokyo</li>
</orgName>
</list>
<tree><country name="Japon"><region name="Région de Kantō"><name sortKey="Trinh, Quang Duy" sort="Trinh, Quang Duy" uniqKey="Trinh Q" first="Quang Duy" last="Trinh">Quang Duy Trinh</name>
</region>
<name sortKey="Hayakawa, Satoshi" sort="Hayakawa, Satoshi" uniqKey="Hayakawa S" first="Satoshi" last="Hayakawa">Satoshi Hayakawa</name>
<name sortKey="Izumi, Yasuyuki" sort="Izumi, Yasuyuki" uniqKey="Izumi Y" first="Yasuyuki" last="Izumi">Yasuyuki Izumi</name>
<name sortKey="Komine Aizawa, Shihoko" sort="Komine Aizawa, Shihoko" uniqKey="Komine Aizawa S" first="Shihoko" last="Komine-Aizawa">Shihoko Komine-Aizawa</name>
<name sortKey="Kuroda, Kazumichi" sort="Kuroda, Kazumichi" uniqKey="Kuroda K" first="Kazumichi" last="Kuroda">Kazumichi Kuroda</name>
<name sortKey="Mizuguchi, Masashi" sort="Mizuguchi, Masashi" uniqKey="Mizuguchi M" first="Masashi" last="Mizuguchi">Masashi Mizuguchi</name>
<name sortKey="Shibata, Toshikatsu" sort="Shibata, Toshikatsu" uniqKey="Shibata T" first="Toshikatsu" last="Shibata">Toshikatsu Shibata</name>
<name sortKey="Shimotai, Yoshitaka" sort="Shimotai, Yoshitaka" uniqKey="Shimotai Y" first="Yoshitaka" last="Shimotai">Yoshitaka Shimotai</name>
<name sortKey="Trinh, Quang Duy" sort="Trinh, Quang Duy" uniqKey="Trinh Q" first="Quang Duy" last="Trinh">Quang Duy Trinh</name>
<name sortKey="Ushijima, Hiroshi" sort="Ushijima, Hiroshi" uniqKey="Ushijima H" first="Hiroshi" last="Ushijima">Hiroshi Ushijima</name>
</country>
<country name="États-Unis"><region name="Connecticut"><name sortKey="Mor, Gil" sort="Mor, Gil" uniqKey="Mor G" first="Gil" last="Mor">Gil Mor</name>
</region>
</country>
</tree>
</affiliations>
</record>
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