| Project/Area Number |
26305017
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 海外学術 |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
阿戸 学 国立感染症研究所, ハンセン病研究センター 感染制御部, 部長 (20392318)
濱野 真二郎 長崎大学, 熱帯医学研究所, 教授 (70294915)
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| Co-Investigator(Renkei-kenkyūsha) |
KANEKO Satoshi 長崎大学, 熱帯医学研究所, 教授 (00342907)
FUJII Yoshito 長崎大学, 熱帯医学研究所, 准教授 (40347498)
OKA Mayuko (OZEKI Yuriko) 京都府立大学, 生命環境科学研究科, 准教授 (00169301)
MAEKURA Ryoji 刀根山病院, 臨床研究部, 副院長 (60423886)
ICHINOSE Yoshio 長崎大学, 熱帯医学研究所, 教授 (70176296)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥16,250,000 (Direct Cost: ¥12,500,000、Indirect Cost: ¥3,750,000)
Fiscal Year 2017: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2016: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2015: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
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| Keywords | 結核 / 感染 / マクロファージ / ケニア / 寄生虫 / コレステロール / HDL / アフリカ / 診断 / 栄養 / 途上国 / 潜在性結核 / HIV |
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| Outline of Final Research Achievements |
This study was performed in tuberculosis-endemic area in Kenya to address molecular mechanisms of latency and know the fundamental knowledge for prediction of disease progression. We found some M. tuberculosis antigens are well recognized by host immune response, while some other antigens were done in individuals with asymptomatic infection. This suggested that detection of the immune responses to M. tuberculosis antigens can be applied for diagnosis of asymptomatic infection and disease progression.
We also found elevated HDL-cholesterol levels in M. tuberculosis-infected individuals. We found human macrophages produces TNF-alpha, a host protective cytokine against tuberculosis, depending on TLR2 upon M. tuberculosis infection. And HDL suppresses TLR2 expression and its cellar signaling. These suggest that higher HDL level may be risk of both asymptomatic and active tuberculosis.
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