| Project/Area Number |
24591152
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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 |
Respiratory organ internal medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
ISHII Yukio 筑波大学, 医学医療系, 教授 (80272194)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 転写因子 / インフルエンザ / レジオネラ肺炎 / 非結核性抗酸菌症 / マクロファージ / Ｔ細胞 / 酸化ストレス / 炎症 / 宿主応答 / 非結核性抗酸菌 / レジオネラ / Ｔ－ｂｅｔ / ＳＱＳＴＭ１ / T細胞 / T-bet / SQSTM1 / 細胞内寄生菌 / ヘルパーＴ細胞 |
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| Outline of Final Research Achievements |
In this study, the protective roles of Nrf2, p62, and T-bet in the development of lung inflammation induced by intracellular pathogens are investigated. Nrf2 is a transcription factor involved in cellular protection against oxidative stimuli. The antioxidant pathway controlled by Nrf2 is found to be pivotal in protection against the development of influenza virus-induced pulmonary inflammation and injury under oxidative conditions.
P62, a scaffold multifunctional protein involved in several cellular events, is found to be a negative regulator of acute pulmonary inflammation during Legionnaires’disease, possibly by regulating inflammasome activity and subsequent proinflammatory cytokine production.
T-bet, the master regulator for Th1 development, is found to be a critical regulator for susceptibility and inflammatory responses to M. avium. T-bet-deficient mice are highly susceptible to M. avium infection with diminishment of Th1 responses and development of Th17 responses.
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