支气管哮喘小鼠支原体感染模型肺组织中T-bet、GATA-3和NF-κB转录因子的变化

Alterations of T-bet, GATA-3 and NF-κB transcription factors in lung tissue of asthmatic mice with Mycoplasma pneumonia infection

目的:检测支气管哮喘支原体肺炎(Mycoplasma pneumonia,MP)感染小鼠模型肺组织的T-box转录因子(T-box expressed in T cells,T-bet)、GATA结合蛋白3(GATA binding protein-3,GATA-3)和核因子-κB(nuclear factor-κB,NF-κB)转录因子的水平,分析支气管哮喘MP感染时这些主要转录因子的变化及其与哮喘发病间的关系。方法:健康雌性BALB/c小鼠,分为卵清白蛋白(ovalbumin,OVA)致敏合并MP感染组(支气管哮喘MP感染组)和OVA致敏组(支气管哮喘组),另设正常对照组,每组15只。运用荧光半定量聚合酶链反应(polymerase chain reaction,PCR)检测各组小鼠模型肺组织中T-bet、GATA-3和NF-κB的表达。结果:支气管哮喘MP感染组和支气管哮喘组小鼠模型肺组织中GATA-3的表达明显高正常对照组(P<0.01),而2组的T-bet表达明显低于正常对照组(P<0.01)。支气管哮喘MP感染组小鼠模型肺组织中NF-κB的表达高于支气管哮喘组及正常对照组(P均<0.01)。结论 :支气管哮喘MP感染小鼠模型肺组织中NF-κB的表达明显升高,MP感染后通过影响与Th2相关的转录因子在哮喘发病中起一定作用。

Objective To detect the expressions of transcription factors T-bet, GATA-3 and NF-κB in lung tissue of asthmatic mice with Mycoplasma pneumonia （MP） infection and analyze the correlation of these transcription factors with pathogenesis of asthma. Methods Forty-five female BALB/c mice wereconstructed as models and divided in 3 groups： OVA and MP infectiongroup, OVA group,and normal control group. Mice in OVA and MP infectiongroup were sensitized byintraperitoneal injection of ovalbuminand given nasal drops of liquid containing MP; mice in OVAGroup were sensitized byintraperitoneal injection of OVA; mice in normal control group weretreated with normal saline.The expressions of T-bet, GATA-3 and NF-κB of lung tissue were measured by fluorescence semi-quantitative PCR. Results Levelsof GATA-3 inOVA and MP infection Group, OVA Group were significantly higher than in that in normal controls, while T-betwere lower than that in normal controls （P〈0.01）. Expression of NF-κB inOVA and MP infection group was higher than that in OVA group and normal control group （P〈0.01）. Conclusions Expression of NF-κB increases in asthmatic mice with MP infection,which indicates that MP infection may play a role in the development of bronchial asthma by influencing the expression of Th2- related transcription factors.