2003 Fiscal Year Final Research Report Summary
Evidence of Platelet-Activating Factor Metabolic Pathway Activation in Human Nasal Mucosa Induced by Allergic Rhinitis
Project/Area Number |
12671690
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Otorhinolaryngology
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Research Institution | Kansai Medical University |
Principal Investigator |
FURUKAWA Masayuki Kansai Medical University, the faculty of medicine, Assistant Proffessor, 医学部, 講師 (00229113)
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Co-Investigator(Kenkyū-buntansha) |
TSUJI Hiroyukib Kansai Medical University, the faculty of medicine, Assosiate Proffessor, 医学部, 助教授 (00155368)
IKEDA Hiroki Kansai Medical University, the faculty of medicine, Assistant, 医学部, 助手 (90288803)
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Project Period (FY) |
2000 – 2003
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Keywords | Platelet-activating factor / Allergic rhinitis / Nasal mucosa / PAF acetyltransferase / Lyso-PAF |
Research Abstract |
Background : Platelet-activating factor (PAP) has a wide range of biological activities. In the lower airways, PAF has been suggested to act as the biochemical mediator partly responsible for bronchial asthma. However, the role of PAF in allergic rhinitis has not been established. Objective : The purpose of this study was to explore the possible role of PAP in the pathogenesis of allergic rhinitis. PAF and PAF-synthesizing enzyme PAF acetyltransferase (PAF-AT) activity in mucosal tissue from patients with allergic rhinitis were investigated. Furthermore, the production of PAF in fresh stimulated nasal mucosa was also studied. Methods : Bioassay for PAF was performed on 7 samples from patients with allergic rhinitis and 3 sample of normal mucosa, and radioimmunoassay for PAF-AT in the microsomal fraction was carried out on 5 samples from patients and normal subjects. Incubation of replicates of fresh nasal mucosa from patients with allergic rhinitis in the presence of calcium ionophore A23187 and antihuman immunoglobline E and the production of PAF were also assayed. Results : PAF was quantitated by platelet-aggrigating activity and found to have 4.56±0.81pg/ μ g phosphorus in nasal mucosal phospholipids (mean±SE, n=7) for patients with allergic rhinitis. In contrast, PAF was near or below the level of detection for the control group. In microsomes from nasal mucosa, specific PAF-AT activity was detected in all samples, and the enzymatic activities were significantly higher in allergic mucosa compared with normal mucosa. Nasal mucosa from patients with allergic rhinitis had the potential to produce PAF upon stimulation. Conclusion : The findings indicate that the metabolic pathway leading to PAF generation is activated during the pathogenesis of allergic rhinitis.
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Research Products
(6 results)