节点文献

肺炎支原体感染对BALB/c小鼠气道IFN-γ和IL-4、IL-5、IL-10以及气道阻力的影响

The effects of mycoplasma pneumonia infection on expressions of IFN-γ, IL-4, IL-5, IL-10 and airway resistance of BALB/c mice

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 张晗焦旭勇尚云晓王莉何梦博韩晓华王桂珍

【Author】 ZHANG Han;JIAO Xu-yong;SHANG Yun-xiao;WANG Li;HE Meng-bo;HAN Xiao-hua;WANG Gui-zhen;Department of Paediatrics, Shengjing Hospital of China Medical University;

【机构】 中国医科大学附属盛京医院小儿呼吸内科中国医科大学基础医学院病原生物学教研室

【摘要】 目的观察肺炎支原体感染对BALB/c小鼠气道IFN-γ和IL-4、IL-5、IL-10以及气道阻力的影响。方法建立肺炎支原体经呼吸道感染的BALB/c小鼠模型,应用RT-PCR和HE染色的方法进行模型的鉴定,用ELLSA的方法检测BALF中细胞因子的含量,AniRes2005动物肺功能仪测各组小鼠肺的吸气阻力、呼气阻力、顺应性。结果 MP感染BALB/c小鼠后IFN-γ和IL-4、IL-5、IL-10细胞因子较正常对照组明显升高(P<0.05);吸气阻力、呼气阻力较正常对照组增加(P<0.05),顺应性降低较正常对照组增加(P<0.05)。结论 MP肺炎感染BALB/c小鼠后气道阻力增加、顺应性降低,而且气道中的炎性因子持续存在。

【Abstract】 Objective To study the the effects of mycoplasma pneumonia(MP) infection on expressions of IFN-γ, IL-4,IL-5, IL-10 and airway resistance of BALB / c mice. Methods The mycoplasma pneumonia infection model was builded by inhalation in BALB / c mouse; The animal model was identified by RT-PCR and HE staining method, the levels of IFN-γ, IL-4, IL-5,IL-10 in bronchoalveolar lavage fluid(BALF) were measured by ELLSA method, inspiratory resistance, expiratory resistance and pulmonary dynamic compliance were detected by AniRes2005 pulmonary function instrument. Results Compared with normal control group, the levels of IFN-γ, IL-4, IL-5, IL-10 in BALF were increased significantly after mycoplasma pneumonia infection, P<0.05; and the inspiratory resistance and expiratory resistance of mice in MP group was lower than mice in normal control group, P<0.05; pulmonary dynamic compliance of mice was lower in MP group than in normal control group. Conclusion The inspiratory resistance and expiratory resistance of mice was increased, pulmonary dynamic compliance was lower after mycoplasma pneumonia infection, and inflammation lasted long enough.

  • 【文献出处】 解剖学研究 ,Anatomy Research , 编辑部邮箱 ,2014年03期
  • 【分类号】R563.1
  • 【被引频次】4
  • 【下载频次】184
节点文献中: 

本文链接的文献网络图示:

本文的引文网络