Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules: University of the Ryukyus Repository


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Title	:	Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules
Authors	:	Teruya, Hiromitsu Tomita, Mariko Senba, Masachika Ishikawa, Chie Tamayose, Maki Miyazato, Akiko Yara, Satomi Tanaka, Yuetsu Iwakura, Yoichiro Fujita, Jiro Mori, Naoki
Issue Date	:	22-Sep-2008
Abstract	:	[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. [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. [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.
URL	:	http://www.retrovirology.com/content/5/1/86
Type Local	:	雑誌掲載論文
ISSN	:	1742-4690
Publisher	:	BioMed Central Ltd.
URI	:	http://hdl.handle.net/20.500.12000/7347
Citation	:	Retrovirology Vol.5 p.86
Appears in Collections	:	Peer-reviewed Journal Articles (Faculty of Medicine)

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