ArticlePloS one2008
SalK/SalR, a two-component signal transduction system, is essential for full virulence of highly invasive Streptococcus suis serotype 2.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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84 citing papers in PubMed, 159 citations in OpenAlex.
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- Encapsulated Streptococcus suis impairs optimal neutrophil functions which are not rescued by priming with colony-stimulating factors.PloS one · 2024Article
- A critical review on experimental Streptococcus suis infection in pigs with a focus on clinical monitoring and refinement strategies.BMC veterinary research · 2023Review
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- Comparative transcriptomic analysis reveal genes involved in the pathogenicity increase ofVirulence · 2022Article
- Comparative analysis of Streptococcus suis genomes identifies novel candidate virulence-associated genes in North American isolates.Veterinary research · 2022Article
- The salivary metatranscriptome as an accurate diagnostic indicator of oral cancer.NPJ genomic medicine · 2021Article
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- Tuning Microbial Activity via Programmatic Alteration of Cell/Substrate Interfaces.Advanced materials (Deerfield Beach, Fla.) · 2021Review
- Streptococcus pyogenes TrxSR Two-Component System Regulates Biofilm Production in Acidic Environments.Infection and immunity · 2021Article
- The type II histidine triad protein HtpsC facilitates invasion of epithelial cells by highly virulent Streptococcus suis serotype 2.Journal of microbiology (Seoul, Korea) · 2021Article
- Pangenome analysis and virulence profiling of Streptococcus intermedius.BMC genomics · 2021Article
- Proposed virulence-associated genes of Streptococcus suis isolates from the United States serve as predictors of pathogenicity.Porcine health management · 2021Article
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- The Impact of SsPI-1 Deletion onPathogens (Basel, Switzerland) · 2019Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStreptococcus suis serotype 2 (S. suis 2, SS2) has evolved into a highly infectious entity, which caused the two recent large-scale outbreaks of human SS2 epidemic in China, and is characterized by a toxic shock-like syndrome. However, the molecular pathogenesis of this new emerging pathogen is still poorly understood. METHODOLOGY/PRINCIPAL
findings89K is a newly predicted pathogenicity island (PAI) which is specific to Chinese epidemic strains isolated from these two SS2 outbreaks. Further bioinformatics analysis revealed a unique two-component signal transduction system (TCSTS) located in the candidate 89K PAI, which is orthologous to the SalK/SalR regulatory system of Streptococcus salivarius. Knockout of salKR eliminated the lethality of SS2 in experimental infection of piglets. Functional complementation of salKR into the isogenic mutant DeltasalKR restored its soaring pathogenicity. Colonization experiments showed that the DeltasalKR mutant could not colonize any susceptible tissue of piglets when administered alone. Bactericidal assays demonstrated that resistance of the mutant to polymorphonuclear leukocyte (PMN)-mediated killing was greatly decreased. Expression microarray analysis exhibited a transcription profile alteration of 26 various genes down-regulated in the DeltasalKR mutant. CONCLUSIONS/SIGNIFICANCE: These findings suggest that SalK/SalR is requisite for the full virulence of ethnic Chinese isolates of highly pathogenic SS2, thus providing experimental evidence for the validity of this bioinformatically predicted PAI.
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