论文部分内容阅读
目的 探讨细胞内信号传导与肺炎链球菌侵袭、致病的关系 ,在体外研究Ⅲ型肺炎链球菌粘附肺Ⅱ型上皮细胞 (A5 49)是否能触发细胞内酪氨酸蛋白激酶 (TPK)信号传导途径 ,以及触发该信号传导可能的细菌亚组分。方法 用FITC荧光标记肺炎链球菌 ,在体外观察肺炎链球菌粘附肺Ⅱ型上皮细胞的粘附动力学特征 ;用免疫组织化学和ELISA方法观察完整细菌触发的细胞内酪氨酸蛋白磷酸化 ,用各种因素预处理肺炎链球菌后 ,观察触发细胞内酪氨酸蛋白磷酸化可能的细菌亚组分。结果 证实了上述粘附过程存在剂量依赖和时间依赖关系 ,而且是特异的过程 ;细菌粘附使细胞内酪氨酸蛋白磷酸化 ,且磷酸化蛋白的产生与粘附具有时间和剂量依赖性。进一步实验证实 :细胞内蛋白酪氨酸磷酸化由细菌表面蛋白质介导。结论 肺炎链球菌粘附肺Ⅱ型上皮细胞能触发细胞内信号传导 ,且细菌表面蛋白质在触发胞内酪氨酸蛋白磷酸化信号传导中起着重要作用。
Objective To investigate the relationship between intracellular signal transduction and invasion and pathogenicity of Streptococcus pneumoniae. To investigate whether type Ⅲ pneumococcal adhesion to lung type Ⅱ epithelial cells (A549) can trigger intracellular tyrosine kinase (TPK) signal The pathways of conduction, and the bacterial sub-components that trigger this signaling. Methods Streptococcus pneumoniae was labeled with FITC to observe the adhesion kinetics of Streptococcus pneumoniae adhesion type Ⅱ epithelial cells in vitro. Immunocytochemistry and ELISA were used to observe the intracellular tyrosine protein phosphorylation triggered by intact bacteria. After pretreatment of S. pneumoniae with various factors, possible bacterial sub-components that trigger intracellular tyrosine protein phosphorylation were observed. The results confirmed that the adhesion process in a dose-dependent and time-dependent, and is a specific process; bacterial adhesion to intracellular tyrosine protein phosphorylation, and phosphorylation of protein production and adhesion with time and dose-dependent. Further experiments confirmed that intracellular protein tyrosine phosphorylation is mediated by bacterial surface proteins. Conclusion Streptococcus pneumoniae adhesion to lung type Ⅱ epithelial cells can trigger intracellular signaling, and bacterial surface proteins play an important role in triggering intracellular tyrosine phosphorylation signaling.