ORIGINAL ARTICLE: H3N2 Influenza A Virus Replicates in Immortalized Human First Trimester Trophoblast Cell Lines and Induces Their Rapid Apoptosis
Identifieur interne : 001165 ( Main/Exploration ); précédent : 001164; suivant : 001166ORIGINAL ARTICLE: H3N2 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 [ 1046-7408 ] ; 2009-09.
Abstract
Problem 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. Method of study 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. Results 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. Conclusion 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:
- https://api.istex.fr/ark:/67375/WNG-CH4D31R4-H/fulltext.pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025808
DOI: 10.1111/j.1600-0897.2009.00723.x
Affiliations:
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Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Mizuguchi, Masashi" sort="Mizuguchi, Masashi" uniqKey="Mizuguchi M" first="Masashi" last="Mizuguchi">Masashi Mizuguchi</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Developmental Medical Sciences, Institute of International Health, Graduate School of Medicine, The University of Tokyo, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName><orgName type="university">Université de Tokyo</orgName></affiliation></author><author><name sortKey="Ushijima, Hiroshi" sort="Ushijima, Hiroshi" uniqKey="Ushijima H" first="Hiroshi" last="Ushijima">Hiroshi Ushijima</name><affiliation wicri:level="3"><country xml:lang="fr">Japon</country><wicri:regionArea>Aino Health Science Center, Aino University, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Mor, Gil" sort="Mor, Gil" uniqKey="Mor G" first="Gil" last="Mor">Gil Mor</name><affiliation wicri:level="2"><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></author><author><name sortKey="Hayakawa, Satoshi" sort="Hayakawa, Satoshi" uniqKey="Hayakawa S" first="Satoshi" last="Hayakawa">Satoshi Hayakawa</name><affiliation wicri:level="3"><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Microbiology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">American Journal of Reproductive Immunology</title><title level="j" type="alt">AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY</title><idno type="ISSN">1046-7408</idno><idno type="eISSN">1600-0897</idno><imprint><biblScope unit="vol">62</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="139">139</biblScope><biblScope unit="page" to="146">146</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2009-09">2009-09</date></imprint><idno type="ISSN">1046-7408</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1046-7408</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Problem 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. Method of study 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. Results 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. Conclusion 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.</div></front></TEI><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 Izawa, Shihoko" sort="Komine Izawa, Shihoko" uniqKey="Komine Izawa 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>Pour manipuler ce document sous Unix (Dilib)
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