| Project/Area Number |
06671703
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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 | Yamanashi Medical University (1996)
Akita University (1994-1995) |
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Principal Investigator |
OKAMOTO Yoshitaka Yamanashi Medical University Professor, 医学部, 教授 (40169157)
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| Co-Investigator(Kenkyū-buntansha) |
伊藤 永子 秋田大学, 医学部, 助手 (90006734)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | nasal mucosa / cytokine / cell adhesion molecule / virus / nasal allergy / chronic sinusitis / ハウスダスト / ヒト鼻アレルギー / トシル酸スプラタスト / マウス / RSウイルス / G糖蛋白 / F糖蛋白 |
|---|
| Research Abstract |
Expression of cytokines and cell adhesion molecules was evaluated in chronic sinusitis and nasal allergy, which are the most popular nasal inflammatory diseases. Also, the effect of viral airway infection on these expressions was investigated.
The results are summarized as follows.
1. Employing specific reverse transcriptase polymerase chain reaction assays, mRNAs of various kinds of cytokines and cell adhesion molecules were detected in maxillary sinus mucosa of the patients with chronic sinusitis. The expression of IL-1alpha, beta was more frequently in acute phase of the disease. The mucosal T cells were thought to play an important role on the expression of these cytokines and on the pathogenesis of the disease. The extracellular matrix may participate in the persistent activation of these T cells.
2. An enhanced expression of the mRNA for various cytokines was observed in nasal mucosal samples of nasal allergic subjects after the administration of allergic antigen or substance P,although the expression of IL-2 and IL-4 was low. These cytokine production may induce the cellular infiltration and the late phase reaction through the activation of cell adhesion molecules. Also, substance P may regulate allergic reaction via enhanced production of certain regulatory cytokines.
3. Respiratory syncytial virus (RSV) enhanced Th-2 like cytokines production but not Th-1 like cytokines production in mitogen stimulated human tonsillar cells. In nasal epithelial cells, RSV induced the expression of intercellular adhesion molecule-1 by itself but not through production of cytokines. The enhanced synthesis of Th-2 like cytokines and cell adhesion molecules in airway infected with RSV may contribute to the unique inflammatory processes.
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