肠炎沙门菌C50336ZinT基因缺失株构建及其相关生物学特性

Construction and biological characteristic of ZinT-deficient mutant of Salmonella enteritidis C50336 strain

为研究锌调控蛋白ZinT在肠炎沙门菌致病中的作用,本试验利用λ-Red同源重组系统构建了肠炎沙门菌(C50336)ZinT基因缺失突变株(C50336ΔZinT),并对其生物学特性进行分析。结果显示,与野生型菌株和回复菌株相比,缺失株C50336ΔZinT在LB培养基中生长速度无明显差异,生化特性亦无明显变化,但其在Minimal培养基中生长明显变慢。此外缺失株C50336ΔZinT对H2O2处理和高渗环境的适应能力显著下降,但在巨噬细胞内的存活率无明显降低。动物试验表明,ZinT基因缺失突变株的毒力和野生型菌株相比仅有轻微下降。本试验探讨了ZinT与肠炎沙门菌锌摄取和毒力间的联系,为进一步阐释肠炎沙门菌感染致病机制奠定基础。

In this study,we examined the role of ZinT in Salmonella enteritidis caused infection with ZinT deleted and tested the biochemical characteristics.The data showed that,the ZinT-knockout did not affect the growth of C50336 strains in LB and change of biochemical characteristics were not observed in ZinT-deletion mutant.Compared to the wild type and complemented strains,the ZinT-deficient mutant displayed sharply impaired survival in minimal medium and significantly increased sensitivity to H2O2 and hypertonic treatment.The similar survival in macrophage and slightly attenuated virulence was observed.This study determined the close relationship of ZinT and Salmonella’s survival under Zn2+-deficient condition,and provided insight into the underlying mechanism of Salmonella caused infection.