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目的观察重组白细胞介素17F(rIL-17F)对肺炎支原体(MP)感染小鼠体内防御素β-2(Defb-2)及巨噬细胞炎性蛋白(MIP)表达的影响,探讨rIL-17F防御MP感染的相关机制。方法 SPF级BALB/c小鼠随机分为感染组、干预组和对照组,以鼻腔接种的方式建立MP感染模型,以鼻腔黏膜免疫方式进行rIL-17F干预。采用荧光定量PCR法检测其肺组织Defb-2、MIP-1α、MIP-2βmRNA的表达水平,ELISA法检测其肺泡灌洗液(BALF)、脾脏及纵隔淋巴结细胞培养上清中MIP-1α、MIP-2β、IL-4、IFN-γ水平。结果 1.干预组MP菌落计数明显低于感染组,BALF中白细胞总数及中性粒细胞、巨噬细胞计数明显高于感染组,差异均有统计学意义。对照组无菌落生长。感染组BALF中白细胞总数及中性粒细胞、巨噬细胞计数明显高于对照组,差异均有统计学意义。2.干预组肺组织Defb-2、MIP-1α和MIP-2βmRNA表达水平均明显高于感染组,差异有统计学意义。3.干预组与感染组比较,MIP-1α水平在纵隔淋巴结细胞培养上清中明显升高,MIP-2β水平在BALF和纵隔淋巴结细胞培养上清中明显升高,差异均有统计学意义;IL-4水平在BALF中明显降低,在脾细胞培养上清中则明显升高,差异均有统计学意义;IFN-γ水平在脾细胞培养上清中明显升高,差异有统计学意义。感染组与对照组比较,MIP-1α水平在脾细胞及纵隔淋巴结细胞培养上清中均明显升高,差异有统计学意义;MIP-2β水平两组之间无显著差异;IL-4水平在BALF及脾细胞培养上清中均明显升高,差异有统计学意义;IFN-γ水平在BALF中明显升高,差异有统计学意义。结论 rIL-17F能促进Defb-2及MIP等炎性因子的表达,调节Th1/Th2平衡,增加感染部位中性粒细胞和巨噬细胞等炎性细胞的聚集,提高MP清除率,增强机体抗感染能力。
Objective To investigate the effect of recombinant interleukin 17F (rIL-17F) on the expression of Defb-2 and MIP in mice infected with Mycoplasma pneumoniae (MP) Defense mechanism of MP infection. Methods SPF BALB / c mice were randomly divided into infection group, intervention group and control group. The model of MP infection was established by nasal inoculation and the intervention of rIL-17F by nasal mucosal immunization. The expression levels of Defb-2, MIP-1α and MIP-2βmRNA in the lung tissue were detected by real-time quantitative PCR. The levels of MIP-1α and MIP in the culture supernatant of BALF, spleen and mediastinal lymph nodes -2β, IL-4, IFN-γ levels. The number of MP colony in the intervention group was significantly lower than that in the infected group. The total number of leucocytes and the neutrophils and macrophages in the BALF were significantly higher than those in the infected group. The differences were statistically significant. The control group grew without colony. The total number of leukocytes and neutrophils and macrophages in BALF in infected group were significantly higher than those in control group, the differences were statistically significant. The expression levels of Defb-2, MIP-1α and MIP-2βmRNA in the lung tissue of the intervention group were significantly higher than those of the infected group, the difference was statistically significant. Compared with the infected group, the level of MIP-1α in the intervention group was significantly increased in the culture supernatant of mediastinal lymph node, and the level of MIP-2βin the BALF and mediastinal lymph node cell culture supernatant was significantly increased, the differences were statistically significant; The level of IL-4 in BALF was significantly decreased in the spleen cell culture supernatant was significantly higher, the difference was statistically significant; IFN-γ levels in the spleen cell culture supernatant was significantly increased, the difference was statistically significant. Compared with the control group, the levels of MIP-1αin the spleen cells and mediastinal lymph node cell culture supernatants were significantly increased, the difference was statistically significant; MIP-2β levels between the two groups no significant difference; IL-4 levels in the BALF and spleen cell culture supernatant were significantly increased, the difference was statistically significant; IFN-γ levels were significantly increased in BALF, the difference was statistically significant. Conclusion rIL-17F can promote the expression of inflammatory factors such as Defb-2 and MIP, regulate the balance of Th1 / Th2, increase the accumulation of inflammatory cells such as neutrophils and macrophages in infected sites, increase the clearance rate of MP and enhance the body resistance Infectious ability.