Examination of the gene therapy for OME using Decoy oligo.

TNF-α诱导或上调腺样体成纤维细胞中IL-8的产生。分泌性中耳炎患者咽鼓管渗出液中IL-8水平与鼓膜顺应性相关，提示增殖体成纤维细胞分泌IL-8是分泌性中耳炎的重要致病因素之一。另外，鼻成纤维细胞中的VCAM-1可通过TNF-α和/或IL-4的刺激来诱导。NF-κB的易位是腺样体成纤维细胞产生IL-8和鼻成纤维细胞产生VCAM-1的关键步骤。基于这些数据，NF-κ B是关键因素，调节这一步骤似乎是治疗OME和CS的新策略。NF-κB诱骗寡核苷酸有望抑制NF-κ IC B易位的激活。采用脂质体法和仙台病毒载体将NF-κ B Decoy oligo转染到体外培养的成纤维细胞中。然而，转染并不成功，我们无法进行将该策略应用于OME小鼠模型的步骤。

TNF-a induced or upregulated IL-8 production in adenoidal fibroblasts. IL-8 level in epipharyngeal effusion and the compliance of tympanic membrane was showed clinically to be correlated in OME, suggesting that I L-8 production from adenoidal fibroblasts is one of the important causative factors of OME. Additionally, VCAM-1 was induced by the stimulation of TNF-a and/or IL-4 in nasal fibroblasts.Translocation of NF-κB is the essential step both in IL-8 production in adenoidal fibroblasts and VCAM-1 production from nasal fibroblasts.Based on these data, NF-κ B is the key factor and the regulation of this step seems to be a new strategy to treat OME and C S.In this project, NF-κB Decoy oligo was expected to suppress the activation of NF-IC B translocation. We applied the liposome method and sendai virus vector to transfect NF-κ B Decoy oligo to cultured fibroblast. However, the transfection was not successful and we could not go to the step of the application of this strategy to the OME mouse model.