spd1672基因敲除显著影响肺炎链球菌的毒力

Spd1672 gene knockout significantly attenuates the virulence of Streptococcus pneumoniae

目的研究spd1672基因在肺炎链球菌感染过程中的作用。方法通过腹腔攻毒实验和细菌入血载量分析、细菌的粘附侵袭实验、全血杀菌实验以及相关细胞因子检测等观察spd1672基因敲除(D39△1672菌株)后对肺炎链球菌毒力的影响。结果D39△1672菌株感染组小鼠中位生存时间和生存率显著高于野生菌株组(P<0.05),而血中细菌载量则显著低于野生菌株感染组(P<0.05)。与野生菌株比较,D39△1672菌株对A549细胞的粘附能力无明显差异,但其侵袭能力显著受损(P<0.05)。此外,D39△1672菌株对全血杀菌作用的抵抗能力亦较野生菌显著减弱(P<0.05),小鼠体内炎性细胞因子水平显著降低。结论spd1672基因与肺炎链球菌的侵袭、抗宿主能力和致炎反应等过程相关。

Objective To investigate the role of spd1672 gene in the infection process of Streptococcus pneumoniae. Methods BALB/ c mice were intraperitoneally infected by a spd1672 knockout strain and a D39 wild-type strain of S. pneumoniae, and the survival time of mice and blood bacterial counts were recorded. The adhesion and invasion ability of S. pneumoniae strains were assessed in A549 cells. Bactericidal assays were carried out to determine the resistance of spd1672 knockout strains and D39 wild strains, and the serum levels of inflammatory cytokines were detected in the infected mice. Results The mice infected with spd1672 knockout strains showed a significantly longer median survival time, a higher survival rate, and a lower blood bacterial load than the wild strain-infected mice （P〈0.05）. Having a similar cell adhesion ability to the wild-type strain （P〉0.05）, the spd1672 knockout strain showed significantly lower cell invasion ability than the wild-type strain （P〈0.05）. The spd1672 knockout strain also had a reduced resistance to whole blood cells, and thw mice infected with spd1672 knockout strain exhibit lower levels of serum inflammatory cytokines than those infected with the wild-type strain. Conclusion Spd1672 gene is importantly related to the virulence of S. pneumoniae and plays important roles in modulating bacterial invasion, resistance to whole blood cells and prolnflammatory responses.