MyD88缺去突变基因转染降低病原菌感染的人呼吸道上皮细胞IL-8的分泌  

Transfection of Dominant Negative MyD88 Decreases IL-8 Production in Bacteria-infected Airway Epithelial Cells

作　　者：冯艳[1] 王芳[1] 陈襄文[1] 冯云[1] 黄宁[1] 王伯瑶[1] 吴琦[1] 

机构地区：[1]四川大学华西医学中心感染免疫教研室,成都610041

出　　处：《生物医学工程学杂志》2006年第5期1092-1095,共4页Journal of Biomedical Engineering

基　　金：国家自然科学基金资助项目(39270688);CMB资助项目(98-681)

摘　　要：白细胞介素-8(1L-8)是呼吸道炎症反应的重要介质。本实验通过构建突变M yD 88真核表达质粒(M yD 88 DN),转染人呼吸道上皮细胞株A 549及SPC-A-1,探讨其对病原菌感染上皮细胞IL-8表达的影响。结果显示:M yD 88 DN转染可降低结核杆菌、绿脓杆菌培养上清诱导的IL-8释放;对肺炎克雷伯杆菌和绿脓杆菌活菌侵袭细胞所刺激的IL-8分泌也有明显的阻断作用。提示突变M yD 88能够阻断细菌感染引起的呼吸道上皮细胞IL-8表达,可能成为呼吸道严重炎症反应基因治疗的新靶基因。Interleukin-8 （IL-8） is an important activator and chemoattratant of neutrophils and has been implicated in airway inflammatory diseases. To explore the new gene therapeutic strategies for airway inflammation, plasmid expressing dominant negative myeloid differentiation protein （MyD88 DN） was constructed and transfected into human airway epithelial cell lines A549 and SPC-A-I. The cells were challenged with M. tuberculosis, P. aeruginosa or K. pneumoniae and the release of IL-8 was measured using ELISA. The results showed that the supernatants of M. tuberculosis and R. aeruginosa enhanced IL-8 release from the epithelial cells and transfection of MyD88 DN diminished this effect. MyD88 DN also reduced IL-8 release from cells induced by live bacteria of P. aeruginosa or K pneumoniae. These data suggest that MyD88 could be used as a target gene in the gene therapy of airway inflammation.

关 键 词：髓样分化蛋白MyD88 白细胞介素-8 呼吸道炎症 基因治疗 

分 类 号：R392[医药卫生—免疫学]