Dexamethasone modulation of MUC5AC and MUC2 gene expression in a generalized model of middle ear inflammation.
Dexamethasone modulation of MUC5AC and MUC2 gene expression in a generalized model of middle ear inflammation.
复制标题
地塞米松对中耳炎症广义模型中 MUC5AC 和 MUC2 基因表达的调节。
DOI：
10.1002/lary.25762
复制
发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Hong,Wenzhou
中科院分区：
文献类型：
--
作者：
Kerschner,JosephE;Khampang,Pawjai;Hong,Wenzhou
目的/假设检测地塞米松对人中耳上皮细胞系（HMEEC-1）中基础和促炎细胞因子诱导的凝胶形成粘蛋白表达的影响。方法将HMEEC-1暴露于促炎细胞因子、肿瘤坏死因子-α（TNF-α）和白细胞介素-1 β（IL-1β）以确定最佳的粘蛋白诱导。HMEEC-1与地塞米松在稳态和存在促炎细胞因子刺激的情况下孵育。结果促炎细胞因子TNF-α和IL-1β诱导HMEEC-1表达MUC 2和MUC 5AC。地塞米松可显著降低MUC 5AC的稳态mRNA水平（P< 0.05），并呈时间和剂量依赖性（P< 0.0001）; MUC 2在各时间点均被有效抑制（P< 0.05）。地塞米松对MUC 2和MUC 5AC的抑制存在时间差异。地塞米松抑制促炎细胞因子诱导的MUC 2和MUC 5AC的表达。结论本研究提供了一个结论性的图片，使用糖皮质激素下调粘蛋白基因表达的能力，使用一个可推广的炎症模型，适用于多种潜在的原因，粘膜肥大。该数据为慢性中耳炎患者未来的干预措施增加了前景。证据等级N/A.Laryngoscope，126：E248-E254，2016
Objectives/HypothesisTo examine the effect of dexamethasone on basal and proinflammatory cytokine‐induced gel‐forming mucin expression in human middle ear epithelial cell line (HMEEC‐1).MethodsHMEEC‐1 was exposed to proinflammatory cytokines, tumor necrosis factor‐alpha (TNF‐), and interleukin‐1 beta (IL‐1β) to identify optimal mucin induction. The HMEEC‐1 was incubated with dexamethasone in the steady state and in the presence of proinflammatory cytokine stimulation. Expression ofMUC2andMUC5ACwas determined by quantitative polymerase chain reaction.ResultsProinflammatory cytokines, TNF‐α and IL‐1β, inducedMUC2andMUC5ACexpression in HMEEC‐1. Dexamethasone reduced steady state mRNA level ofMUC5ACin a time‐dependent (P< 0.05) and dose‐dependent (P< 0.0001) manner.MUC2was effectively suppressed at all time points tested (P< 0.05). Temporal difference between dexamethasone suppression ofMUC2andMUC5ACwas demonstrated. Dexamethasone inhibits the proinflammatory cytokine‐induced expression of bothMUC2andMUC5AC.ConclusionThis work provides a conclusive picture of the ability of using glucocorticoids to downregulate mucin gene expression in human MEE using a generalizable model of inflammation that is applicable to multiple potential causes of MEE mucosal hypertrophy. This data adds to the promising potential of future interventions for patients with chronic otitis media.Level of EvidenceN/A.Laryngoscope, 126:E248–E254, 2016