Item type |
デフォルトアイテムタイプ(フル)(1) |
公開日 |
2008-10-03 |
タイトル |
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タイトル |
Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules |
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言語 |
en |
作成者 |
Teruya, Hiromitsu
Tomita, Mariko
Senba, Masachika
Ishikawa, Chie
Tamayose, Maki
Miyazato, Akiko
Yara, Satomi
Tanaka, Yuetsu
Iwakura, Yoichiro
Fujita, Jiro
Mori, Naoki
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
[Background] Human T-cell leukemia virus type I (HTLV-I) is associated with pulmonary diseases, characterized by bronchoalveolar lymphocytosis, which correlates with HTLV-I proviral DNA in carriers. HTLV-I Tax seems to be involved in the development of such pulmonary diseases through the local production of inflammatory cytokines and chemokines in T cells. However, little is known about induction of these genes by HTLV-I infection in lung epithelial cells. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
[Results] We tested infection of lung epithelial cells by HTLV-I by coculture studies in which A549 alveolar and NCI-H292 tracheal epithelial cell lines were cocultured with MT-2, an HTLV-I-infected T-cell line. Changes in the expression of several cellular genes were assessed by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay and flow cytometry. Coculture with MT-2 cells resulted in infection of lung epithelial cells as confirmed by detection of proviral DNA, HTLV-I Tax expression and HTLV-I p19 in the latter cells. Infection was associated with induction of mRNA expression of various cytokines, chemokines and cell adhesion molecule. NF-κB and AP-1 were also activated in HTLV-I-infected lung epithelial cells. In vivo studies showed Tax protein in lung epithelial cells of mice bearing Tax and patients with HTLV-I-related pulmonary diseases. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
[Conclusion] Our results suggest that HTLV-I infects lung epithelial cells, with subsequent production of cytokines, chemokines and cell adhesion molecules through induction of NF-κB and AP-1. These changes can contribute to the clinical features of HTLV-I-related pulmonary diseases. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
論文 |
出版者 |
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言語 |
en |
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出版者 |
BioMed Central Ltd. |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ |
journal article |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
出版タイプ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
識別子 |
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識別子 |
http://hdl.handle.net/20.500.12000/7347 |
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識別子タイプ |
HDL |
関連情報 |
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識別子タイプ |
URI |
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関連識別子 |
http://www.retrovirology.com/content/5/1/86 |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
10.1186/1742-4690-5-86 |
関連情報 |
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識別子タイプ |
PMID |
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関連識別子 |
18808681 |
収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1742-4690 |
収録物識別子 |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA12051445 |
収録物名 |
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言語 |
en |
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収録物名 |
Retrovirology |
書誌情報 |
巻 5,
p. 86,
発行日 2008-09-22
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