Kerschner Joseph E, Khampang Pawjai, Hong Wenzhou
Division of Pediatric Otolaryngology , Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin, U.S.A.
Department of Otolaryngology and Communication Sciences , Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin, U.S.A.
Laryngoscope. 2016 Jul;126(7):E248-54. doi: 10.1002/lary.25762. Epub 2015 Nov 3.
OBJECTIVES/HYPOTHESIS: To examine the effect of dexamethasone on basal and proinflammatory cytokine-induced gel-forming mucin expression in human middle ear epithelial cell line (HMEEC-1).
HMEEC-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 of MUC2 and MUC5AC was determined by quantitative polymerase chain reaction.
Proinflammatory cytokines, TNF-α and IL-1β, induced MUC2 and MUC5AC expression in HMEEC-1. Dexamethasone reduced steady state mRNA level of MUC5AC in a time-dependent (P < 0.05) and dose-dependent (P < 0.0001) manner. MUC2 was effectively suppressed at all time points tested (P < 0.05). Temporal difference between dexamethasone suppression of MUC2 and MUC5AC was demonstrated. Dexamethasone inhibits the proinflammatory cytokine-induced expression of both MUC2 and MUC5AC.
This 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.
N/A. Laryngoscope, 126:E248-E254, 2016.
目的/假设：研究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黏蛋白表达的影响。
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-1β（IL-1β），以确定最佳的黏蛋白诱导情况。将HMEEC-1在稳态以及存在促炎细胞因子刺激的情况下与地塞米松一起孵育。通过定量聚合酶链反应测定MUC2和MUC5AC的表达。
促炎细胞因子TNF-α和IL-1β诱导了HMEEC-1中MUC2和MUC5AC的表达。地塞米松以时间依赖性（P < 0.05）和剂量依赖性（P < 0.0001）方式降低了MUC5AC的稳态mRNA水平。在所有测试时间点，MUC2均受到有效抑制（P < 0.05）。显示了地塞米松对MUC2和MUC5AC抑制的时间差异。地塞米松抑制促炎细胞因子诱导的MUC2和MUC5AC的表达。
本研究使用一种适用于多种中耳黏膜肥大潜在病因的通用炎症模型，确凿地展示了糖皮质激素下调人中耳黏蛋白基因表达的能力。该数据为慢性中耳炎患者未来的干预措施增添了有前景的潜力。
无。《喉镜》，2016年，第126卷，E248-E254页
