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SoxS is a positive regulator of key pathogenesis genes and promotes intracellular replication and virulence of Salmonella Typhimurium.
Microb Pathog. 2020 Feb; 139:103925.MP

Abstract

Salmonella enterica serovar Typhimurium (S. Typhimurium) is an important intracellular pathogen, causing gastroenteritis or severe systemic infection in a variety of hosts. During infection, S. Typhimurium must survive and replicate in host macrophages, which produce abundant oxidative compounds. SoxRS regulon is a well-known regulator that is activated in response to oxidative stress and promotes bacterial tolerance to oxidants in E. coli. However, the global regulatory function of SoxS in S. Typhimurium remains poorly characterized. Here, we used an RNA sequencing-based approach to investigate the role of SoxS in the expression of S. Typhimurium virulence genes. Besides the downregulation of genes related to resistance to oxidative stress, we found that in a soxS deletion mutant the expression of Salmonella pathogenicity island (SPI)-2 genes, which are crucial for replication within macrophages, was significantly repressed. Moreover, immunofluorescence and mice infection experiments showed that soxS deletion inhibited replication in macrophages and decreased virulence upon intraperitoneal inoculation in mice, respectively. Collectively, our findings demonstrate that SoxS is a positive regulator of SPI-2 genes and, therefore, plays a crucial role in S. Typhimurium intracellular replication and virulence.

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Authors+Show Affiliations

Wang P
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China; College of Life Sciences, Nankai University, Tianjin, 300071, China.
Zhang H
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China; College of Life Sciences, Nankai University, Tianjin, 300071, China.
Liu Y
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China; College of Life Sciences, Nankai University, Tianjin, 300071, China.
Lv R
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China.
Liu X
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China.
Song X
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China; College of Life Sciences, Nankai University, Tianjin, 300071, China.
Wang J
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China.
Jiang L
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, 300457, China; Tianjin Key Laboratory of Microbial Functional Genomics, Tianjin, 300457, China; The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, 300457, China. Electronic address: jianglingyan@nankai.edu.cn.

MeSH

AnimalsBacterial ProteinsFemaleGene Expression Regulation, BacterialGenomic IslandsHumansMiceMice, Inbred BALB CSalmonella InfectionsSalmonella typhimuriumTrans-ActivatorsVirulence

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31838175

Citation

Wang, Peisheng, et al. "SoxS Is a Positive Regulator of Key Pathogenesis Genes and Promotes Intracellular Replication and Virulence of Salmonella Typhimurium." Microbial Pathogenesis, vol. 139, 2020, p. 103925.
Wang P, Zhang H, Liu Y, et al. SoxS is a positive regulator of key pathogenesis genes and promotes intracellular replication and virulence of Salmonella Typhimurium. Microb Pathog. 2020;139:103925.
Wang, P., Zhang, H., Liu, Y., Lv, R., Liu, X., Song, X., Wang, J., & Jiang, L. (2020). SoxS is a positive regulator of key pathogenesis genes and promotes intracellular replication and virulence of Salmonella Typhimurium. Microbial Pathogenesis, 139, 103925. https://doi.org/10.1016/j.micpath.2019.103925
Wang P, et al. SoxS Is a Positive Regulator of Key Pathogenesis Genes and Promotes Intracellular Replication and Virulence of Salmonella Typhimurium. Microb Pathog. 2020;139:103925. PubMed PMID: 31838175.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - SoxS is a positive regulator of key pathogenesis genes and promotes intracellular replication and virulence of Salmonella Typhimurium. AU - Wang,Peisheng, AU - Zhang,Huan, AU - Liu,Yutao, AU - Lv,Runxia, AU - Liu,Xiaoqian, AU - Song,Xiaorui, AU - Wang,Jingting, AU - Jiang,Lingyan, Y1 - 2019/12/12/ PY - 2019/7/1/received PY - 2019/12/11/revised PY - 2019/12/11/accepted PY - 2019/12/16/pubmed PY - 2020/10/27/medline PY - 2019/12/16/entrez KW - Intracellular replication KW - RNA sequencing KW - Salmonella pathogenicity island-2 genes KW - Salmonella typhimurium KW - SoxS KW - Virulence SP - 103925 EP - 103925 JF - Microbial pathogenesis JO - Microb Pathog VL - 139 N2 - Salmonella enterica serovar Typhimurium (S. Typhimurium) is an important intracellular pathogen, causing gastroenteritis or severe systemic infection in a variety of hosts. During infection, S. Typhimurium must survive and replicate in host macrophages, which produce abundant oxidative compounds. SoxRS regulon is a well-known regulator that is activated in response to oxidative stress and promotes bacterial tolerance to oxidants in E. coli. However, the global regulatory function of SoxS in S. Typhimurium remains poorly characterized. Here, we used an RNA sequencing-based approach to investigate the role of SoxS in the expression of S. Typhimurium virulence genes. Besides the downregulation of genes related to resistance to oxidative stress, we found that in a soxS deletion mutant the expression of Salmonella pathogenicity island (SPI)-2 genes, which are crucial for replication within macrophages, was significantly repressed. Moreover, immunofluorescence and mice infection experiments showed that soxS deletion inhibited replication in macrophages and decreased virulence upon intraperitoneal inoculation in mice, respectively. Collectively, our findings demonstrate that SoxS is a positive regulator of SPI-2 genes and, therefore, plays a crucial role in S. Typhimurium intracellular replication and virulence. SN - 1096-1208 UR - https://www.unboundmedicine.com/medline/citation/31838175/SoxS_is_a_positive_regulator_of_key_pathogenesis_genes_and_promotes_intracellular_replication_and_virulence_of_Salmonella_Typhimurium_ DB - PRIME DP - Unbound Medicine ER -