@techreport{oai:mie-u.repo.nii.ac.jp:00008030,
 author = {竹内, 万彦 and TAKEUCHI, KAZUHIKO and 石永, 一 and ISHINAGA, HAJIME and 坂井田, 寛 and SAKAIDA, HIROSHI},
 month = {May},
 note = {application/pdf, 好酸球性副鼻腔炎では非好酸球性副鼻腔炎粘膜と比べてTGF-α 蛋白の発現が増加していた。ヒト上皮細胞株ではTGF-αはERKシグナリング経路を用いてTNF-αと相乗的にMUC5ACの発現を亢進させた。IL-31および１IL-31受容体はアレルギー性鼻炎において発現が亢進しており、MUC5AC遺伝子の発現を亢進させた。抗菌作用をもたない新規エリスロマイシン誘導体のEM900はIL-1βで惹起されたMUC5ACムチン遺伝子の発現亢進を有意に抑制した。この作用はEM900がNF-κB活性化を抑制することによってもたらされた。, TGF-α immunoreactivity was found markedly increased in the submucosal tissue in the eosinophilic chronic rhinosinusitis patient compared with that of a normal patient and with noneosinophilic chronic rhinosinusitis. TGF-α synergized with TNF-α to upregulate MUC5AC expression in human epithelial cells through the ERK signaling pathway. IL-31 and IL-31RA are upregulated in patients with allergic rhinitis, and induce MUC5AC gene expression in human airway epithelial cells. These findings suggest that IL-31 plays an important role in mucus overproduction in nasal allergic inflammation. A new erythromycin derivative, EM900, does not have antibacterial action. EM900 suppressed induction of inflammatory cytokines and MUC5AC gene expression in cells derived from human airway epithelia, and our findings indicated that these effects may be mediated by the suppression of NF-κB activation., 2010年度～2012年度科学研究費補助金(基盤研究(C))研究成果報告書, 22591899},
 title = {上気道の難治病態における粘液分泌過多の機序の解明とその制御},
 year = {2013}
}