| Project/Area Number |
12671676
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
|
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
HIMI Tetsuo Sapporo Medical University, School of Medicine, Professor, 医学部, 教授 (90181114)
|
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| Co-Investigator(Kenkyū-buntansha) |
北 秀明 札幌医科大学, 医学部, 助手 (00305228)
上村 正見 札幌医科大学, 医学部, 助手 (60311891)
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| Project Period (FY) |
2000 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
|
| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Innate Immunity / Infectious disease / Drug resistance / TLR / signal transduction / 生体防御機構 / サイトカイン / 細菌抗原 / 鼻咽腔 |
|---|
| Research Abstract |
The inflammatory mediators are intimately involved in the inflammatory cascade occurring in the upper air way and middle ear. Recent evidence reveals that innate immunity has an important role to play in the initial defense mechanisms. The innate immune system identifies bacteria by means of a pattern-recognition receptor. Mammalian Toll-like receptors (TLRs) are considered to be key receptors in this system. Stimulation of target cells with bacterial component results in a TLR-dependent the activation of NF kappa B leading to the production of pro-inflammatory cytokines. In this study, the production of cytokines, induced by representative pathogens and their components, was studied using not only animal model but also effector cell lines. The relationship between pathogens and TLR2 was also elucidated. Moreover, we referred to a new species of middle ear pathogen, Alloiococcus otitidis.
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