皮肤屏障功能破坏、金葡菌定植引起抗原持续刺激、肥大细胞相关炎症因子表达水平失衡进而导致持续性炎症反应是特应性皮炎（AD）发病的关键因素。本项目组在应用利多卡因静脉封闭治疗重症AD取得较好疗效的基础上，证实利多卡因在体外可上调皮肤屏障功能关键物质抗菌肽HBD-3的表达水平。那么与抗菌肽密切相关的肥大细胞相关炎症因子的表达水平是否受到利多卡因的调控？其机制是什么？本研究旨在①探讨利多卡因对HBDs刺激后的肥大细胞系LAD2所分泌的炎症因子的表达是否具有调控作用，并明确其信号通路；②探讨利多卡因治疗前后人体及金葡菌诱导的AD小鼠模型中HBDs和肥大细胞相关炎症因子的表达水平。

Skin barrier dysfunction, constant antigenic stimulation of Staphylococcus aureus colonization and abnormal expression of mast cell relative inflmmatory factors contribute to the pathogenesis of atopic dermatitis (AD). In view of the good curative effect of lidocaine in the clinical practice with severe AD patients, we carried out the research. It was proven that lidocaine could up-regulate the expression of HBD-3 in vitro, which is a critical factor of skin barrier function. HBDs were identified to be closely associated with the expression of mast cell realtive inflmmatory factors. Then the regulation of lidocaine on the expression of mast cell realtive inflmmatory factors and the specific pathway of regulation by lidocaine remained unknown. Our amis of the research are as follows: 1) We plan to verify the regulatory function of lidociane on the mast cell line LAD2 with the stimulation of HBDs and define the specific pathway. 2) We aim to invetigate the expression of HBDs and mast cell realtive inflmmatory factors in human and staphylococcal enterotoxin sensitized murine models which accept the lidocaine therapy.