1991 Fiscal Year Final Research Report Summary
Study on the mechanism of host defense against MAC infection
| Project/Area Number |
02670342
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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 Kyoto University, Chest Disease Research Institute Infection and Inflammation, Professor, 胸部疾患研究所, 教授 (10027104)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Katsuhiro Kyoto University, Chest Disease Research Institute Infection and Inflammation, Instructor, 胸部疾患研究所, 助手 (00206468)
TANAKA Eisaku Kyoto University, Chest Disease Research Institute Infection and Inflammation, Instructor, 胸部疾患研究所, 助手 (30183461)
AMITANI Ryoichi Kyoto University, Chest Disease Research Institute Infection and Inflammation, Lecturer, 胸部疾患研究所, 講師 (70167964)
SUZUKI Yasuhiro Kyoto University, Chest Disease Research Institute Molecular Pathology, Professor, 胸部疾患研究所, 教授 (90027110)
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| Project Period (FY) |
1990 – 1991
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| Keywords | M. avium complex / Macrophage / Cytokine / BRM / Granuloma / Corticosteroid / New Rifamycin |
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| Research Abstract |
(1)We investigated the cell population in the lung lesion of murine model of M. avium complex(MAC)infection by total pulmonary lavage and immunohistochemistry. At the 9th week of infection when granuloma formation were completed, CD8+ lymphocytes were predominant in the lesion outside the granuloma, while CD4+ lymphocytes were predominant in the granuloma.
(2)We investigated the effect of several cytokines on anti-MAC activities of human alveolar macrophages(PAM)in vitro. GM-CSF and TNF-alpha could activate PAM to inhibit growth of MAC.
(3)We investigated the effect of TNF-alpha and TNF-beta on antiMAC activities in vivo. Injection of TNF-alpha enhanced the resistance against MAC infection in a murine model.
(4)We examined the effect of the combination of corticosteroid with new rifamycin, KRM1648. The combination therapy reduced more numbers of viable bacilli in the lung than the treatment of KRM1648 alone.
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