| Project/Area Number |
12670566
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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 | University of the Ryukyus |
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Principal Investigator |
SAITO Atushi University of the Ryukyus, Professor, 医学部, 教授 (90039842)
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| Co-Investigator(Kenkyū-buntansha) |
KOIDE Michio UNIVERSITY OF THE RYUKYUS, Instructor, 医学部, 助手 (40234679)
HIGA Futoshi HOSPITAL OF UNIVERSITY OF THE RYUKYUS, Instructor, 医学部・付属病院, 助手 (50291555)
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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 |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Legionella pneumonia / Legionella longbeachae / apoptosis / cytotoxicity / bacterial growth in host cells / caspase / TNF-α / FAS / Legionella pneumophila |
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| Research Abstract |
The cytotoxicity of the facultative intracellular bacterium, Legionella longbeachae, an important cause of legionellosis, was characterised. Apoptosis was induced in HL-60 cells, a human macrophage-like cell line, during the early stages of infection and induction of apoptosis correlated with cytotoxicity. Apoptosis was confirmed by agarose gel electrophoresis of fragmented DNA, surface exposure of phosphatidylserine, and propidium-iodide labelling of host cell nuclei. The involvement of Mip (macrophage infectivity potentiator) protein, a known virulence factor of L. longbeachae, was also examined. A mip mutant of L. longbeachae induced apoptosis of HL-60 cells but failed to multiply intracellularly, suggesting that intracellular replication of L. longbeachae is not essential for the induction of apoptosis of HL-60 cells. Furthermore, induction of apoptosis of L. longbeachaeinfected macrophages was mediated by activation of the caspase pathway but might be independent of TNF-α and Fas-mediated signal-transduction pathways.
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