| Project/Area Number |
25860296
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Experimental pathology
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| Research Institution | Nara Medical University (2014)
Okayama University (2013) |
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Principal Investigator |
ITO TOSHIHIRO 奈良県立医科大学, 医学部, 教授 (00595712)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | エピジェネティクス / インフルエンザウィルス / 気道上皮細胞 / マクロファージ / ヒストンメチル化 |
|---|
| Outline of Final Research Achievements |
Influenza A virus causes acute respiratory infections that induce annual epidemics and occasional pandemics. Especially, the main cause of death in influenza viral infection is secondary bacterial pneumonia. Both bronchial epithelial cells and macrophages upregulated SET domain, bifurcated 2 (SETDB2) expression following influenza virus H1N1 infection. SETDB2 is a histone methyltransferase that methylates Lys-9 of histone H3 (H3K9), which is correlated with repression of transcription. SETDB2 expression is dependent on RIG-I induced type-I IFN pathway. Moreover, SETDB2 regulates TRAF2, an adaptor molecule of TNF signaling, and amphiregulin, which plays a critical role for promoting the restoration of airway epithelial integrity and lung tissue homeostasis.
These findings indicate that SETDB2 regulation might be one of the critical therapeutic target for influenza virus infection and secondary bacterial pneumonia.
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