Contribution of nadR to the cell growth and virulence of Streptococcus suis serotype 2

文献类型： 外文期刊

第一作者： Guo, Genglin

作者： Guo, Genglin;Zhang, Yuhang;Wei, Dan;Yu, Yanfei;Zhang, Wei;Zhang, Yuhang;Wei, Dan;Zhang, Wei;Zhang, Yuhang;Wei, Dan;Zhang, Wei;Zhang, Yuhang;Wei, Dan;Li, Quan;Zhang, Wei;Yu, Yanfei;Yu, Yanfei

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关键词： Streptococcus suis; NadR; Cell growth; Virulence

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.3； 五年影响因子：3.5 ）

ISSN： 0378-1135

年卷期： 2024 年 288 卷

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收录情况： SCI

摘要： Streptococcus suis serotype 2 (SS2) has been reported to be a highly invasive pathogen in swine and a zoonotic agent for humans. Although many bacterial virulence factors have been identified, our an insightful under-standing of SS2 pathogenicity is lacking. The gene nadR, encoding nicotinamide-nucleotide adenylyltransferase, was first reported as a regulator and transporter of the intracellular NAD synthesis pathway in Salmonella typhimurium. In this study, we constructed a mutant strain of nadR (AnadR) to test the phenotypic and virulence variations between the deletion mutant and the wild-type strain ZY05719. The phenotypic experimental results showed that AnadR obviously inhibited cell growth and exhibited shorter chains than WT. The growth defect of AnadR was caused by the loss of the function of nadR for transporting the substrates nicotinamide mono-nucleotide and nicotinamide riboside in the intracellular NAD synthesis pathway. In the process of interaction with the host, AnadR participated in adherence and invasion to the host cells, and it was more easily cleared by RAW264.7 macrophages. More importantly, both zebrafish and BALB/c mice in vivo virulence experimental results showed that AnadR dramatically attenuated the virulence of SS2, and the ability of AnadR to colonize tissues was notably reduced in comparison with that of WT in the BALB/c mice infection model. To the best of our knowledge, this is the first time to demonstrate that nadR not only plays an important role in bacterial growth, but also in connection with the virulence of SS2 as a global transcriptional regulator.

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