| Project/Area Number |
15H06372
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
Okuno Tatsusada 大阪大学医学系研究科, 助教 (00464248)
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ミトコンドリアＤＮＡ / 視神経脊髄炎 / 自然免疫 / ミトコンドリアDNA / オートファジー / アストロサイト |
|---|
| Outline of Final Research Achievements |
Mitochondrial DNA (mtDNA),one of damage-associated molecular patterns, has been reported to stimulate innate immunity. Recent studies suggest that activation of innate immunity occurs in the acute phase of NMOSD. We measured mtDNA levels in cerebrospinal fluid of NMOSD and compared to these of multiple sclerosis and other neurological diseases (ONDs) using quantitative PCR. We stimulated mouse primary astrocyte cultures with AQP4-Ab and measured the level of mtDNA in the supernatant. We added DNA fraction from the culture supernatant to microglia cultures, and measured IL-1β in the supernatants. The level of mtDNA was significantly higher in patients with acute NMOSD than remission NMOSD, acute MS, and ONDs. mtDNA level was increased in the supernatant of astrocyte cultures stimulated with AQP4-Ab. We also demonstrated that mtDNA promoted IL-1β secretion from microglia.
AQP4-Ab promotes mtDNA release from astrocytes. Our results suggests that mtDNA might be involved in NMOSD pathogen
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