| Project/Area Number |
20390167
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Yasuko 京都大学, 医学研究科, 助教 (00331869)
FUNATO Tadao 東北福祉大学, 健康科学部, 教授 (70165455)
伊藤 弘康 岐阜大学, 医学研究科, 講師 (80373075)
清島 満 岐阜大学, 医学研究科, 教授 (10171315)
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| Co-Investigator(Renkei-kenkyūsha) |
ITO Hiroyasu 岐阜大学, 医学研究科, 講師 (80373075)
SEISHIMA Mitsuru 岐阜大学, 医学研究科, 教授 (10171315)
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| Project Period (FY) |
2008 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2010: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2009: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2008: ¥9,880,000 (Direct Cost: ¥7,600,000、Indirect Cost: ¥2,280,000)
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| Keywords | 臨床検査医学 / 生理活性物質 / サイトカイン / 炎症・免疫 / 臨床化学 |
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| Research Abstract |
The role of indoleamine 2, 3-dioxygenase(IDO) in the L-tryptophan(Trp)-kynurenine(Kyn) pathway after viral infection was investigated. We used IDO deficient(IDO^-/-) mice and mice treated with 1-methyl-D, L-Trp(1-MT), an inhibitor of IDO, to study the importance of Trp-Kyn pathway metabolites. After viral infection(i. e myocarditis virus), the levels of Kyn increased, while those of Trp decreased, and IDO activity increased in the tissues. The survival rate of IDO^-/-or 1-MT-treated mice was significantly greater than that of IDO^+/+ mice. Indeed, the viral load was suppressed in the IDO^-/-or 1-MT-treated mice. Furthermore, the levels of type I interferons in IDO^-/-mice were significantly higher than those in IDO^+/+ mice, and treatment of IDO^-/-mice with Kyn metabolites eliminated the effects of IDO^-/-on the improved survival rates. Our findings show that Kyn metabolites regulate the production of type I IFNs by decreasing the number macrophages. Consequently, modulation of the Trp-Kyn pathway may be an effective strategy for treating certain viral infectious diseases.
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