| Project/Area Number |
61570372
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
KUZE Fumiyuki M.D. Professor, Chest Disease Research Institute, Kyoto University, 胸部疾患研究所, 教授 (10027104)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Kokichi M.D. Instructor, Research Reacter Institute, Kyoto University., 原子炉実験所, 助手 (10166796)
SUZUKI Yasuhiro M.D. Professor, Chest Disease Research Institute, Kyoto University., 胸部疾患研究所, 教授 (90027110)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1988: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | M. intracellulare infection mouse model / monoclonal antibody / acquired immune deficiency / Cellular immunity / 細胞性免疫 / 非定型抗酸菌症 |
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| Research Abstract |
Recently many patients with acquired immune deficiency syndrome (AIDS) were reported to have frequent Mycobacterium intracellulare infection. But the treatment of both of them were quite unsatisfactory. We have established the M.intracellulare infection mouse model, and by using it, have investigated about the treatment of its infection further. For the purpose of establish the immune deficiency model, nomoclonal anti-mouse Thy1.2 antibody was administered to the M.intracellulare infection model mice. but unsatisfied immune depression was earned. So we decided to investigate the inflammatory cell dynamics for the mycobacterial infection at first. Inflammatory cells were recovered by total pulmonary lavage (TPL) and stained with monoclonal anti-Thy1.2, Lyt-2(CD8), L3T4(CD4), and Ia. The cell surface antigen expression were measured by flow cytometrical cell analizer. Tpls were performed during the course of infection. Thy1.2 positive and Lyt-2 positive lymphocytes were increased soon after the infection, but the L3T4 positive lymphocytes and Ia positive macrophages were gradually increased three weeks after infection. Thy1.2 positive lymphocytes and Ia positive macrophages reached the plateau six weeks after infection. On the contraty, Lyt-2 positive and L3T4 positive lymphocytes were up and down with their surface antigen expression ratio and have a contra-rotation course as if they were feed back controlled each other. For the next step, the effects of biological response modifiers (BRMs) were investigated. Recombinant interleukin-2 (rIL-2), Muramyl dipeptide derivative; DJ-7041 and cyclosporin A (CyA) were administered to the M.intracellulare infection mice. The increase of Ia positive macrophages at the early stage after infection by rIL-2 treated mice and at the late stage by DJ-7041 treated mice were observed. By using this model we are going to establish the immune deficiency mouse model akin to the AIDS with M.intracellulare infection.
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