| Project/Area Number |
15390516
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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 | Mie University |
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Principal Investigator |
MAJIMA Yuichi Mie University, Faculty of Medicine, Professor, 医学部, 教授 (60024791)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEUCHI Kazuhiko Mie University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (50206942)
YUTA Atsushi Mie University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (80293778)
清水 猛史 三重大学, 医学部附属病院, 助教授 (00206202)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥13,000,000 (Direct Cost: ¥13,000,000)
Fiscal Year 2004: ¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 2003: ¥8,700,000 (Direct Cost: ¥8,700,000)
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| Keywords | chronic sinusitis / allergic rhinitis / nasal polyposis / remodeling / submucosal gland / mucus / extracellular matrix / animal model / 鼻 / 副鼻腔 / ムチン遺伝子 / 気道分泌 |
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| Research Abstract |
Remodeling of the nose and the paranasal sinuses was investigated in the patients with chronic sinusitis(CS) and with allergic rhinitis(AR). In nasal and/or sinus mucosa of CS and AR, the proliferation of submucosal gland cells were remarkable. The mucous cells and the serous cells were increased in CS and AR, respectively. Endoscopic sinus surgery(ESS) significantly reduced the proliferated mucous cells in CS. Loss of cilia also recovered in the sinus mucosa of CS after ESS. Thickening of nasal mucosa by deposition of extracellular matrix was observed in CS. These results indicate that remodelings are remarkable in CS and AR, and some of the remodelings could be reversible. Arachidonic acid metabolites, cysLTs, upregulated mucin gene expressions. Another arachidonic acid metabolite, PGE2, downregulated mucus production through PGE2 receptors (EPS,EP4). It is well known that histamine promotes mucus hypersecretion through Hi receptor. However histamine inhibited mucus production through H3 receptors. Thrombin, a serine protease in human serum, promoted mucus production, enhanced epithelial permeability and upregulated VEGF and TGF-β production from epithelial cells. EM703, a 14-membered macrolide antibiotics without antibacterial activities, inhibited mucus production. A cysLT1 receptor antagonist inhibited mucin gene expression by inhibiting Raf-1MEK/2-ERK1/2-pp90rsk signaling pathway. Our results show a clue as to the regulation of mucus hypersecretion from proliferated secretory cells.
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