BPIFB1在铜绿假单胞菌引起的炎症反应中的调节作用

发布时间：2018-06-02 03:55

本文选题：BPIFB + 脂多糖　；参考：《细胞与分子免疫学杂志》2013年06期

【摘要】：目的研究杀菌性/通透性增强蛋白折叠结构1(BPIFB1)在铜绿假单胞菌引起的炎症反应中的作用机制和调节途径。方法应用RNA干涉、特异性蛋白激酶抑制剂阻断法,通过ELISA、Western blot法测定BPIFB1与脂多糖(LPS)共同作用于RAW264.7细胞后膜表面CD14、TLR受体以及胞内相关信号转导通路分子表达水平的变化情况。结果 BPIFB1与LPS作用后RAW264.7细胞表面CD14、TLR4和MyD88的表达水平明显下降;当细胞中MyD88、TRAF6、NF-κB等蛋白分子的表达被各自特异性siRNA所阻断后,BPIFB1与LPS抑制细胞因子TNF-α过表达的能力也被显著抑制;当用BPIFB1与LPS处理过的细胞用相应蛋白激酶抑制剂作用后,细胞内相关通路蛋白p38、pERK1/2、Akt1磷酸化水平被明显抑制。结论 BPIFB1与LPS结合通过阻抑相关胞内细胞因子的表达,降低了铜绿假单胞菌所产生的细胞炎性反应程度。
[Abstract]:Objective to study the mechanism and regulatory pathway of bactericidal / permeability enhancing protein folding structure (BPIFB1) in inflammatory response induced by Pseudomonas aeruginosa (Pseudomonas aeruginosa). Methods RNA interference and specific protein kinase inhibitor blocking were used to detect the expression of CD14TLR receptor and intracellular signal transduction pathway molecules on the surface of RAW264.7 cells treated with BPIFB1 and lipopolysaccharide (LPS) by EISA-Western blot. Results the expression levels of CD14TLR4 and MyD88 on RAW264.7 cells were significantly decreased after the treatment of BPIFB1 with LPS, and the ability of BPIFB1 and LPS to inhibit the overexpression of TNF- 伪 was also significantly inhibited when the expression of protein molecules such as MyD88-TRAF6NF- 魏 B was blocked by specific siRNA. When the cells treated with BPIFB1 and LPS were treated with the corresponding protein kinase inhibitor, the phosphorylation level of p38 pERK1 / 2 + Akt1 was significantly inhibited. Conclusion BPIFB1 combined with LPS can inhibit the expression of intracellular cytokines and decrease the degree of cellular inflammatory response induced by Pseudomonas aeruginosa.
【作者单位】：沈阳医学院病原生物学教研室;沈阳医学院沈洲医院;沈阳医学院临床医学系;
【基金】：国家自然科学基金(81172509) 沈阳医学院优秀人才启动基金(20113064)
【分类号】：R392-33

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