可溶性TLR4/MD-2体外对炎症反应的抑制作用  

Roles of soluble TLR4/MD-2 complex in preventing excessive inflammatory response in vitro

作　　者：杜本军[1] 高全胜[2] 马洪滨[3] 

机构地区：[1]南方医科大学南方医院整形外科,广州510282 [2]军事医学科学院实验动物中心,北京100071 [3]解放军302医院临床检验医学中心,北京100039

出　　处：《军事医学》2011年第2期115-117,157,共4页Military Medical Sciences

基　　金：国家自然科学基金资助项目(30900313)

摘　　要：目的探讨利用可溶性TLR4受体复合物(TLR4/MD-2)阻断LPS/TLR-4信号通路,缓解过度炎症反应的可行性及其机制。方法用大肠杆菌K12感染正常人外周血的方法建立体外感染模型,观察加入可溶性TLR4/MD-2受体复合物后炎症介质IL-6、IL-8以及中性粒细胞表面CD11b、巨噬细胞表面CD80等的表达变化。结果与结论可溶性TLR4/MD-2受体复合物能显著降低细菌感染后炎症性细胞因子IL-6、IL-8的分泌水平,以及炎症细胞表面共刺激分子的表达。可溶性TLR4/MD-2能有效阻断体外感染模型中炎症介质的释放,为探索新的炎症性损伤防治途径提供了实验依据。Objective To test the roles of soluble TLR4/MD-2 complex in blocking LPS/TLR4 signal pathway and in preventing LPS induced excessive inflammation.Methods An ex vivo infection model was established by adding K12 bacteria to human blood cells according to the published method.Then the roles of soluble TLR4/MD-2 complex in preventing cytokine production and co-stimulatory molecular expression were evaluated by ELISA and flow cytometry respectively.Results and Conclusion K12 infection induced excessive pro-inflammatory cytokine production and up-regulated co-stimulatory molecules expression.Soluble TLR4/MD-2 complex significantly down-regulated the production of IL-6,IL-8,decreased the expression of CD11b on neutrophils and CD80 on macrophage induced by K12 infection.Soluble TLR4/MD-2 complex can be used as a feasible regent to prevent inflammatory injury caused by bacterial infections in vitro.

关 键 词：重组TLR4 LPS 感染 炎症控制 

分 类 号：R363[医药卫生—病理学]