| Project/Area Number |
23390398
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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 |
Otorhinolaryngology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
HIMI Tetsuo 札幌医科大学, 医学部, 教授 (90181114)
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| Co-Investigator(Kenkyū-buntansha) |
TAKANO Kenichi 札幌医科大学, 医学部, 講師 (70404689)
OHKUNI Tsuyoshi 札幌医科大学, 医学部, 助教 (40464490)
SEKI Nobuhiko 札幌医科大学, 医学部, 助教 (30404693)
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| Co-Investigator(Renkei-kenkyūsha) |
TSUTSUMI Hiroyuki 札幌医科大学, 医学部, 教授 (80217348)
KOJIMA Takashi 札幌医科大学, 医学部, 教授 (30260764)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2013: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2012: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2011: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | 鼻粘膜 / 上皮細胞 / アレルギー / ウイルス / タイト結合 / 樹状細胞 / 呼吸器ウイルス / 細胞間接着装置 / クルクミン / フムロン / 自然免疫 / 鼻粘膜上皮 / RSウイルス / 上皮バリア / インターフェロン |
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| Research Abstract |
The mucosal barrier of the upper respiratory tract including the nasal cavity, which is the first site of exposure to inhaled antigens, plays an important role in host defense in terms of innate immunity and is regulated in large part by tight junctions of epithelial cells. Tight junction molecules are expressed in both M cells and dendritic cells as well as epithelial cells of upper airway. Various antigens are sampled, transported, and released to lymphocytes through the cells in nasal mucosa while they maintain the integrity of the barrier. Expression of tight junction molecules and the barrier function in normal human nasal epithelial cells are affected by various stimuli including growth factor, TLR ligand, and cytokine. In addition, epithelial-derived cytokines, enhances the barrier function together with an increase of tight junction molecules in HNECs. Furthermore, RSV infection in HNECs in vitro induces the barrier function together with proinflammatory cytokine release.
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