College of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Jiangsu Co-innovation Center for the Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, China.
Virulence. 2021 Dec;12(1):1538-1549. doi: 10.1080/21505594.2021.1936770.
() is an important rising pathogen that causes serious diseases in humans and pigs. Although some putative virulence factors of have been identified, its pathogenic mechanisms are largely unclear. Here, we identified a putative virulence-associated factor MutT, which is unique to serotype 2 (SS2) virulent strains. To investigate the biological roles of MutT in the SS2 virulent strain ZY05719, the knockout mutant (Δ) was generated and used to explore the phenotypic and virulent variations between the parental and Δ strains. We found that the mutation significantly inhibited cell growth ability, shortened the chain length, and displayed a high susceptibility to HO-induced oxidative stress. Moreover, this study revealed that MutT induced the adhesion and invasion of SS2 to host cells. Deletion of increased microbial clearance in host tissues of the infected mice. Sequence alignment results suggested that was encoded in a strain-specific manner, in which the detection was strongly linked to bacterial pathogenicity. In both zebrafish and mice infection models, the virulence of Δ was largely reduced compared with that of ZY05719. Overall, this study provides compelling evidence that MutT is indispensable for the virulence of SS2 and highlights the biological role of MutT in bacteria pathogenesis during infection.
（）是一种重要的新兴病原体，可导致人类和猪患严重疾病。尽管已经确定了一些假定的毒力因子，但该病原体的致病机制在很大程度上仍不清楚。在这里，我们鉴定了一个假定的与毒力相关的因子 MutT，它是血清型 2（SS2）毒力株所特有的。为了研究 MutT 在 SS2 毒力株 ZY05719 中的生物学作用，我们生成了 MutT 的缺失突变株（Δ），并用于探索亲本株和Δ株之间的表型和毒力变化。我们发现，MutT 的突变显著抑制了细胞生长能力，缩短了链长，并表现出对 HO 诱导的氧化应激的高度敏感性。此外，本研究揭示了 MutT 诱导 SS2 对宿主细胞的黏附和侵袭。在感染小鼠的组织中，缺失 MutT 增加了微生物的清除。序列比对结果表明，MutT 是在菌株特异性的方式下编码的，其检测与细菌致病性密切相关。在斑马鱼和小鼠感染模型中，与 ZY05719 相比，Δ的毒力大大降低。总的来说，这项研究提供了确凿的证据表明 MutT 对于 SS2 的毒力是不可或缺的，并强调了 MutT 在感染期间细菌发病机制中的生物学作用。
