Lin J, Haruta A, Kawano H, Ho S B, Adams G L, Juhn S K, Kim Y
Otitis Media Research Center, Department of Otolaryngology, University of Minnesota School of Medicine, Minneapolis, MN 55455, USA.
J Infect Dis. 2000 Sep;182(3):882-7. doi: 10.1086/315767. Epub 2000 Aug 17.
Mucoid otitis media (MOM) is characterized by viscous fluid, high in mucin concentration, which accumulates in the middle ear cavity. Recent studies suggest that initial infection in the middle ear cleft may be key to the development of MOM. However, factors of the initial infection attributed to the stimulation of mucin production are not clearly understood. This study demonstrated that tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine in mucoid effusion, markedly increased Muc2 mucin mRNA expression in middle ear epithelium, in a time- and dose-dependent manner. Parallel to this was a marked increase in mucin glycoprotein in middle ear fluid. Also, TNF-alpha demonstrated an autocrine and/or paracrine effect on the expression of endogenous TNF-alpha gene in the middle ear, which may contribute to the production of mucin in this study. These findings suggest that TNF-alpha plays an important role in the development of MOM by stimulating mucin metabolism.
胶耳的特征是中耳腔内积聚了黏蛋白浓度很高的黏性液体。最近的研究表明，中耳裂的初始感染可能是胶耳发病的关键。然而，导致黏蛋白产生受刺激的初始感染因素尚不清楚。本研究表明，肿瘤坏死因子（TNF）-α是一种存在于黏液性渗出液中的促炎细胞因子，它能以时间和剂量依赖的方式显著增加中耳上皮细胞中Muc2黏蛋白的mRNA表达。与此同时，中耳液中的黏蛋白糖蛋白也显著增加。此外，TNF-α对中耳内源性TNF-α基因的表达具有自分泌和/或旁分泌作用，这可能在本研究中促进了黏蛋白的产生。这些发现表明，TNF-α通过刺激黏蛋白代谢在胶耳的发病过程中起重要作用。
