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

doi:10.1186/1742-4690-5-86

Retrovirology

Volume 5

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Teruya H
Tomita M
Senba M
Ishikawa C
Tamayose M
Miyazato A
Yara S
Tanaka Y
Iwakura Y
Fujita J
Mori N

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Teruya H
Tomita M
Senba M
Ishikawa C
Tamayose M
Miyazato A
Yara S
Tanaka Y
Iwakura Y
Fujita J
Mori N
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Research

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

Hiromitsu Teruya¹^,2 , Mariko Tomita¹ , Masachika Senba³ , Chie Ishikawa¹^,4^,5 , Maki Tamayose² , Akiko Miyazato⁶ , Satomi Yara² , Yuetsu Tanaka⁷ , Yoichiro Iwakura⁸ , Jiro Fujita² and Naoki Mori¹

¹Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa, Japan

²Division of Control and Prevention of Infectious Diseases, Graduate School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa, Japan

³Department of Pathology, Institute of Tropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki, Japan

⁴Division of Child Health and Welfare, Faculty of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa, Japan

⁵The Japanese Society for the Promotion of Science (JSPS), Japan

⁶Department of Infectious Diseases and Infection Control, International Medical Center, Saitama Medical School, 1397-1 Yamane Hidaka, Saitama, Japan

⁷Division of Immunology, Faculty of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa, Japan

⁸Center for Experimental Medicine, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan

author email corresponding author email

Retrovirology 2008, 5:86doi:10.1186/1742-4690-5-86


Published:	22 September 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.