| Project/Area Number |
12670271
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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 |
Bacteriology (including Mycology)
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
KURA Fumiaki National Institute of Infectious Diseases, Department of Bacteriology, Senior Research Scientist (30161722)
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| Co-Investigator(Kenkyū-buntansha) |
AMEMURA-MAEKAWA Junko Natianal Institute of Infectious Diseases, Department of Bacteriology, Research Scientist (20238843)
TSUKANO Hiroko National Institute of Infectious Diseases, Department of Bacteriology ; Chief, Laboratory of Systemic Infection (50072955)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Legionella / macrophages / natural resistance / microglia |
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| Research Abstract |
Two types of response against microbial infections have been known, acquired-resistance through cell-mediated immunity and natural resistance. Legionella pneumophila (Lp), an intracellular bacterium, causes severe pneumonia in compromised humans. In this study, we examined protective factors against Legionella infection using Lgnl-congenic mice, which are different in the capability of macrophages to restrict Lp growth, and knockout mice defective in production of bactericidal active oxygen species. (1) We examined bacterial modulation of host response using immunomagnetic beads with live or heat-killed Lp. The immunomagnetic beads were phagocytosed by peritoneal macrophages from A/J mice (Lgnl^s) in vitro culture. The macrophages were harvested and homogenized. The phagosomes from the macrophages were collected using a magnet and their components were analyzed by electrophoresis and western blotting. A subunit of NADPH oxidase was decreased in the phagosomes with live Lp but not in those with heat-killed Lp, suggesting the possibility that Lp suppresses the integrity and the activity of NADPH oxidase in Lp-harboring phagosomes. (2) Lp burden in lungs was comparable between wild and myeloperoxidase (MPO)-knockout C57B1/6 mice (Lgnl^r) after intranasal infection. However, in Lgnl^s mice of A/J background, MPO-knockout mice revealed more bacterial growth in lungs. In the situation that Lp can multiply in macrophages, neutrophil MPO was suggested to contribute to the protection against Lp infection, in an addition to NADPH oxidase.
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