论文部分内容阅读
【目的】探索假想脂蛋白连接酶(putative lipoate-protein ligase,LPL)对肺炎链球菌毒力的影响。【方法】采用长臂同源多聚酶链式反应(LFH-PCR)的方法失活lpl基因,通过PCR、测序鉴定缺陷菌株,采用细胞实验比较缺陷菌和野生菌对宿主细胞的粘附能力,并通过动物实验观察lpl基因缺陷后菌株毒力的变化。【结果】小鼠毒力实验表明野生菌株和缺陷株半数致死时间均为12h,两者比较无统计学差异;缺陷菌在对宿主细胞的粘附能力明显高于野生菌株(P<0.01);体外荚膜染色实验表明,野生菌和缺陷菌均有荚膜。【结论】实验结果提示lpl基因对细菌粘附宿主细胞有抑制作用,但不影响其腹腔感染小鼠的能力。
【Objective】 To explore the effect of putative lipoate-protein ligase (LPL) on the virulence of Streptococcus pneumoniae. 【Method】 The lpl gene was inactivated by long-arm homologous polymerase chain reaction (LFH-PCR). Defect strains were identified by PCR and sequencing. Cell adhesion experiments were performed to compare the host cell adhesion ability of the defective and wild strains. To observe the changes of virulence of strains after lpl gene deficiency by animal experiments. 【Results】 The virulence of mice showed that the lethal time of the wild strain and the defective strain was 12 h. There was no significant difference between the two strains. The adhesion ability of the defective bacteria to the host cell was significantly higher than that of the wild strain (P <0.01). In vitro capsular staining experiments showed that both wild and defective bacteria capsular. 【Conclusion】 The results suggest that the lpl gene can inhibit bacterial adhesion to host cells, but does not affect the ability of mice to infect abdominal cavity.