| Project/Area Number |
15K21562
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
Immunology
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| Research Institution | Fukuoka University |
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Principal Investigator |
ITOH Ryota 福岡大学, 医学部, 助教 (70403920)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | クラミジア / マクロファージ / 脂質 / スカベンジャー受容体 |
|---|
| Outline of Final Research Achievements |
The obligate intracellular pathogens Chlamydia pneumoniae is well known to the common cause of respiratory tract diseases and has been associated with development of atherosclerosis. For optimal chlamydial growth, prompt modifications of host intracellular environment by C. pneumoniae, for example controlling of inflammation, enzyme activation or metabolism are important. We showed that C. pneumoniae infection to murine bone marrow macrophages (BMMs) induced the differentiation to inflammatory macrophages, and sequentially redifferentiated to anti-inflammatory macrophages. Some scavenger receptors were induced during first differenciation and promoted lipid uptake of infected BMMs. Lysosomal acid lipase (LAL) is also induced by C. pneumoniae infection and may steers the differentiation of anti-inflammatory macrophage. These multi-step differentiation and induction of a series of metabolic enzyme may increase the intracellular nutrients and provide the optimal growth of C. pneumoniae.
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