| Project/Area Number |
15K10348
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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 |
Neurosurgery
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| Research Institution | Kindai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
義江 修 近畿大学, 医学部, 教授 (10166910)
中田 晋 京都薬科大学, 薬学部, 准教授 (80590695)
宮武 伸一 大阪医科大学, 医学部, 特別職務担当教員(教授) (90209916)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | グリオーマ / 放射線脳壊死 / マクロファージ / 免疫チェックポイント分子 / 腸内細菌叢 / 遅発性脳放射線壊死 / 慢性炎症 / M2 マクロファージ |
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| Outline of Final Research Achievements |
In M2 macrophages accumulating in radioactive necrotic brain tissues, immunosuppressive molecules such as B7-H3 and B7-H5 were found to be upregulated. Likewise, in the mouse model, the expression of these molecules was also enhanced, and they were found to be involved in peripheral edema of radiation brain necrosis. Analysis of intestinal microflora in mice using the next generation sequencer showed that Clostridia correlated with the intensity of the immune response related to cerebral radiation necrosis. M2 removal experiment showed marked prolongation of mouse survival days. These results suggest that M2 macrophages and intestinal bacteria infiltrating into tissues are involved in the deterioration of cerebral radiation necrosis.
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