| Project/Area Number |
23790473
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Bacteriology (including Mycology)
|
|---|
| Research Institution | Hamamatsu University School of Medicine |
|---|
Principal Investigator |
SETO Shintaro 浜松医科大学, 医学部, 助教 (50383203)
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 結核菌 / マクロファージ / オートファジー / イメージ解析 / プロテオミクス / 樹状細胞 |
|---|
| Research Abstract |
Mycobacterium tuberculosis is an intracellular bacterium that can survive within macrophages. Such survival is potentially associated with Coronin-1a. We investigated the mechanism by which Coronin-1a promotes the survival of M. tuberculosis in macrophages and found that autophagy was involved in the inhibition of mycobacterial survival in Coro1a knockdown macrophages. Fluorescence microscopy and immunoblot analyses revealed that LC3, a representative autophagic protein, was recruited to M. tuberculosis-containing phagosomes in Coro1a knockdown macrophages. Thin-section electron microscopy demonstrated that bacilli were surrounded by the multiple membrane structures in Coro1a knockdown macrophages. These results demonstrate the formation of autophagosomes around M. tuberculosis in Coro1a knockdown macrophages. LC3 recruitment to M. Tuberculosis-containing phagosomes was also observed in Coronin-1a knockdownalveolar or bone marrow derived macrophages. These results suggest that Coronin-1ainhibits autophagosome formation in alveolar macrophages, thereby facilitating M. tuberculosis survival within the lung.
|
