| Project/Area Number |
10671602
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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 | KUMAMOTO UNIVERSITY |
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Principal Investigator |
KEISAKE Masuyama Kumamoto University, School of Medicine, Associate Professor, 医学部, 助教授 (30181663)
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| Co-Investigator(Kenkyū-buntansha) |
中崎 孝志 熊本大学, 医学部・附属病院, 助手 (30315303)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2000: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | allergic rhinitis / histamine hyperresponsiveness in the nasal mucosa / PAF / in situ hybridization / trigeminal ganglion cell / 鼻腺 |
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| Research Abstract |
To clarify histamine hyperreactivity of nasal mucosa in allergic rhinitics, we have examined the effect of inflammatory mediators such as PAF, TXA2, and LTC4 on histamine H1 receptor mRNA expression of rat trigeminal ganglion cells or nasal mucosa with an application of in situ hybridization technique.
PAF induced increased histamine H1 receptor mRNA expression in trigeminal ganglion cells. The effect was not induced by lyso-PAF, and abolished by the pretretment with WEB2086, PAF receptor-antagonists. These results indicated that it was mediated by specific PAF recepors. After 30 minute stimulation with PAF, histamine H1 receptor mRNA was enhanced at 1 to 8 hour incubation period of time, peaked at 4 hour and diminised at 24 hour in organ culture. Further, the effect was induced by a relatively low range of concentrations of PAF (10^<-9>-10^<-12>M), suggesting the possibility of its occurence in vivo. In contrast, LTC4 and TXA2 failed to induce histamine H1 recptor mRNA expression in trigeminal ganglia.
PAF also induced histamine H1 recptor mRNA expression in nasal glands, but LTC4/TXA2 did not. These resluts suggest that PAF stimulation of sensory nerve endings or nasal glands underlies the upregulation of H1 receptor expression and this induces histamine hyperresponsiveness in the nasal mucosa.
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