| Project/Area Number |
24590502
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Parasitology (including Sanitary zoology)
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| Research Institution | Gunma University |
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Principal Investigator |
Shimada Junko 群馬大学, 保健学研究科, 教授 (20211964)
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| Co-Investigator(Kenkyū-buntansha) |
HATABU Toshimitsu 岡山大学, 農学部, 准教授 (60344917)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | オートファジー / 南米型トリパノソーマ / 宿主-寄生虫相互作用 / トリパノソーマ / アポトーシス / オートファゴソーム / 宿主応答 / エルサルバドル |
|---|
| Outline of Final Research Achievements |
Autophagy has emerged as an essential component of the defense system against intracellular pathogens. We demonstrated that Trypanosoma cruzi, an intracellular protozoan parasite, was not eliminated by host autophagic machinery. Puncta of LC3, an autophagy marker, were significantly increased after the infection, indicating that T. cruzi infection activated the early step of host autophagy. However, the degradation of p62, with a known marker in autolysosome formation, and autolysosomes were not observed in the infected cells. These results indicated that T. cruzi infection inhibits host autophagy pathway before the autolysosome formation. Furthermore, autophagosome formation was inhibited at the step of conversion from LC3-Atg3 to LC3-Ⅱin T. cruzi infected cells.
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