ArticlePloS one2013
The putative thiosulfate sulfurtransferases PspE and GlpE contribute to virulence of Salmonella Typhimurium in the mouse model of systemic disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Article
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- A widespread bacterial protein compartment sequesters and stores elemental sulfur.Science advances · 2024Article
- The Role of Egg Yolk in Modulating the Virulence ofFrontiers in cellular and infection microbiology · 2022Article
- Genetic Determinants of Stress Resistance in Desiccated Salmonella enterica.Applied and environmental microbiology · 2021Article
- Global responses to oxytetracycline treatment in tetracycline-resistant Escherichia coli.Scientific reports · 2020Article
- Investigating host-bacterial interactions among enteric pathogens.BMC genomics · 2019Article
- Article
- Computational Analysis of Host-Pathogen Protein Interactions between Humans and Different Strains of EnterohemorrhagicFrontiers in cellular and infection microbiology · 2017Article
- Salmonella Typhimurium undergoes distinct genetic adaption during chronic infections of mice.BMC microbiology · 2016Article
- Importance of sigma factor mutations in increased triclosan resistance in Salmonella Typhimurium.BMC microbiology · 2015Article
- Article
- Salmonella-how a metabolic generalist adopts an intracellular lifestyle during infection.Frontiers in cellular and infection microbiology · 2014Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phage-shock protein PspE and GlpE of the glycerol 3-phosphate regulon of Salmonella enterica serovar Typhimurium are predicted to belong to the class of thiosulfate sulfurtransferases, enzymes that traffic sulfur between molecules. In the present study we demonstrated that the two genes contribute to S. Typhimurium virulence, as a glpE and pspE double deletion strain showed significantly decreased virulence in a mouse model of systemic infection. However, challenge of cultured epithelial cells and macrophages did not reveal any virulence-associated phenotypes. We hypothesized that their contribution to virulence could be in sulfur metabolism or by contributing to resistance to nitric oxide, oxidative stress, or cyanide detoxification. In vitro studies demonstrated that glpE but not pspE was important for resistance to H2O2. Since the double mutant, which was the one affected in virulence, was not affected in this assay, we concluded that resistance to oxidative stress and the virulence phenotype was most likely not linked. The two genes did not contribute to nitric oxid stress, to synthesis of essential sulfur containing amino acids, nor to detoxification of cyanide. Currently, the precise mechanism by which they contribute to virulence remains elusive.
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