| Project/Area Number |
13670601
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | SHIMANE MEDICAL UNIVERSITY |
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Principal Investigator |
SATO Katsumasa SHIMANE MEDICAL UNIVERSITY, MICROBIOLOGY AND IMMUNOLOGY, INSTURUCTOR, 医学部, 助手 (00142331)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Toshiaki SHIMANE MEDICAL UNIVERSITY, MICROBIOLOGY AND IMMUNOLOGY, INSTURUCTOR, 医学部, 助手 (60284030)
TOMIOKA Haruaki SHIMANE MEDICAL UNIVERSITY, MICROBIOLOGY AND IMMUNOLOGY, PROFESSOR, 医学部, 教授 (40034045)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | M.tuberculosis / M.avium complex / type II alveolar pneumocytes / lymphocytes / macrophages / A-549 cells / PBMC / cytokines / M. avium complex / リンパ酸 |
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| Research Abstract |
Our previous study revealed that both Mycobacterium tuberculosis (MTB) and M.avium complex (MAC) organisms invade type II alveolar epithelial cells in the lungs when mice are subjected to mycobacterial challenge via the intracheal route. In addition, MTB- or MAC-infected A-549 human type II alveolar epithelial cells (A-549 cells) release humoral factors (TNF-α and GM-CSF), thereby increasing antimycobacterial activity of macrophages(Mφs). In this study, the following findings have been obtained. (1) Anti-TNF-α and anti-GM-CSF antibodies attenuated A-549 cell-dependent inhibition of the intramacrophage growth of MTB and MAC, indicating crucial roles of these cytokines in A-549 cell-mediated potentiation of Mφ antimycobacterial activity. (2) When human peripheral blood mononuclear cells (PBMC) were added onto MTB-infected A-549 cells and Con A- or PPD-induced T cell mitogenesis was examined, T cell mitogenosis in the presence of A-549 cells was inhibited more profoundly than cases without A-549 cells. Such an inhibitory effect was also observed for A-549 cells without MTB infection. When a dual chamber system was used to prevent the cell contact between PBMC and A-549 cells, similar results were also obtained. Therefore, it is thought that the observed inhibition of PBMC mitogenesis due to A-549 cells is dependent upon some unknown humoral T cell-inhibitory factors released from A-549 cells.
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