【摘要】 目的探讨Toll样受体2(TLR2)-髓样分化因子88(MyD88)-核转录因子κB(NF-κB)信号通路在支原体肺炎(MPP)小鼠肺部炎症损伤中的作用及其机制。方法健康SPF级BALB/c小鼠60只,随机分为MPP组(40只),对照组(20只),MPP组采用支原体菌液滴鼻至下呼吸道的方法建立支原体肺炎小鼠模型,对照组采用等量的生理盐水按上述同样方法处理。肺炎支原体(MP)感染后第7天,观察两组小鼠肺组织的病理变化;通过称量小鼠肺组织及体质量计算两组小鼠湿肺质量指数;采用ELISA法测定两组小鼠肺泡灌洗液中白细胞介素4(IL-4)、IL-6的含量;采用免疫组化方法检测两组小鼠肺组织中TLR2和TLR4、MyD88、NF-κB的表达。结果光镜下MPP组小鼠肺组织出现肺泡结构破坏、炎性细胞浸润等情况;对照组小鼠肺组织结构基本正常。MP感染后第7天,MPP组小鼠湿肺质量指数明显高于对照组(t=316.03,P<0.01)。MPP组小鼠肺泡灌洗液中IL-4、IL-6表达水平明显高于对照组(t=7.46、33.97,P<0.01)。MPP组小鼠肺组织中TLR2、TLR4、MyD88、NF-κB表达水平明显高于对照组(t=7.95～11.70,P<0.01)。结论 MP感染后可能通过TLR-MyD88-NF-κB信号通路诱导肺部炎症反应并加重肺损伤。更多还原

【Abstract】 Objective To investigate the role and mechanism of the Toll-like receptor 2(TLR2)-myeloid differentiation factor-88(MyD88)-nuclear factor-kappa B(NF-κB) signaling pathway in pulmonary inflammatory injury in mice with Mycoplasma pneumoniae pneumonia(MPP). Methods A total of 60 healthy specific pathogen-free BALB/c mice were randomly divided into MPP group with 40 mice and control group with 20 mice. The mice in the MPP group were given intranasal administration of mycoplasma bacterial solution to the lower respiratory tract to establish a mouse model of MPP, and those in the control group were gi-ven an equal volume of normal saline using the same method. On day 7 after Mycoplasma pneumoniae infection, pathological changes of the lungs were observed for the two groups; lung tissue was weighed and body weight was measured to calculate wet lung weight index; ELISA was used to measure the levels of interleukin-4(IL-4) and interleukin-6(IL-6) in bronchoalveolar lavage fluid; immunohistochemistry was used to measure the expression of TLR2, TLR4, MyD88, and NF-κB in lung tissue. ResultsUnder a light microscope, the MPP group showed alveolar structural destruction and inflammatory cell infiltration in lung tissue, while the control group showed a basically normal structure of lungs. On day 7 after Mycoplasma pneumoniae infection, the MPP group had a significantly higher lung index than the control group(t=316.03,P<0.01). Compared with the control group, the MPP group had significantly higher levels of IL-4 and IL-6 in bronchoalveolar lavage fluid(t=7.46,33.97,P<0.01) and expression levels of TLR2, TLR4, MyD88, and NF-κB in lung tissue(t=7.95-11.70,P<0.01). Conclusion Mycoplasma pneumoniae may induce pulmonary inflammatory reaction and aggravate lung injury via the TLR-MyD88-NF-κB signaling pathway after infection.更多还原