Treg在大鼠重症肺炎克雷伯菌肺炎中的调控作用

Role of Treg in the mouse severe Klebsiella pneumonia

目的确定CD4+CD25+Treg调节性T细胞在重症肺炎克雷伯菌肺炎中的表达以及意义,探讨CD4+CD25+Treg在重症肺炎克雷伯菌肺炎的免疫抑制中的调控作用。方法通过气管内滴注肺炎克雷伯菌菌液建立重症肺炎模型。采用流式细胞仪检测CD4+CD25+Treg细胞及酶联免疫吸附法(ELISA)等方法检测各种细胞因子。结果重症肺炎克雷伯菌肺炎大鼠的脾脏和肺中CD4+CD25+Treg的数量增加。使用了CD25抗体(PC61)去除机体内源性的CD4+CD25+Treg,分别去除脾脏和肺的94%和90%的CD4+CD25+Treg。CD25抗体组在建模4 h,12 h及24h后,肺部MPO及血清IL-1,IL-6,MIP-2较对照组高(P<0.05),肺和BLA比对照组高(P<0.05),CD25抗体组大鼠生存率比对照组低(P<0.05)。结论内源的CD4+CD25+Treg对大鼠抑制重症肺炎克雷伯菌肺炎的过度免疫损害反应起到保护作用。

Objective To confirm the expression and meaning of the T regular cell in the severe Klebsiella pneumonia, and to evaluate the regular and control affect in the immunologic suppression of the severe Klebsiella pneumonia. Methods To build the severe pneumonia model by intratracheally inoculated with Klebsiella pneumoniae bacteria.To check sorts of inflamma-tion factors by the methods of ELISA and flow cytometry. Results The quantity of the CD4 ＋CD25 ＋Treg in the splenic and lungs of the mice with severe Klebsiella pneumonia were increased.Anti-CD25Ab （PC61 ）was used to remove endogenous CD4 ＋CD25 ＋Treg.Anti-CD25 treatment remove 90% of CD4 ＋CD25 ＋Treg cells.The cytokine production （IL-1β,IL-6,MIP-2）in the anti-CD25-treated group were significantly increased.And it also increased significantly in the airway neutrophil infil-tration,while the survival rate had been decreased. Conclusion Endogenous CD4 ＋CD25 ＋Treg can provide obvious protection effect to the restraining the over immunity damage of the severe Klebsiella pneumonia for the mice.