ArticleVirulence2018
The VraSR regulatory system contributes to virulence in Streptococcus suis via resistance to innate immune defenses.
Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
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- Innate immune response to Streptococcus suis infection: advances and future challenges.Veterinary research · 2026Review
- SSU_RS09155, a virulence-associated gene encoding a putative membrane of unknown function, that is essential for Streptococcus suis serotype 2 virulence.Veterinary research · 2026Article
- Mechanistic Landscape and Farm to Fork Control Strategies forTransboundary and emerging diseases · 2026Review
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- NO Synthesis in Immune-Challenged Locust Hemocytes and Potential Signaling to the CNS.Insects · 2021Article
- The Role and Regulatory Network of the CiaRH Two-Component System in Streptococcal Species.Frontiers in microbiology · 2021Review
- Resistome ofACS infectious diseases · 2020Article
- Transcriptome Analysis of Gene Expression inMicroorganisms · 2020Article
- Identification of an Autorepressing Two-Component Signaling System That Modulates Virulence in Streptococcus suis Serotype 2.Infection and immunity · 2019Article
- VraSR and Virulence Trait Modulation during Daptomycin Resistance in Methicillin-ResistantmSphere · 2019Article
- The VraSR regulatory system contributes to virulence in Streptococcus suis via resistance to innate immune defenses.Virulence · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus suis is a highly invasive pathogen that can cause sepsis and meningitis in pigs and humans. However, we have limited understanding of the mechanisms S. suis uses to evade innate immunity. To investigate the involvement of the two-component signal transduction system of S. suis in host immune defense, we examined the expression of 15 response regulators of S. suis following stimulation with polymorphonuclear leukocytes (PMNs). We found that several response regulators were significantly up-regulated including vraR. Thus, we constructed an isogenic deletion mutant of vraSR genes in S. suis and demonstrated VraSR promotes both bacterial survival in human blood and resistance to human PMN-mediated killing. The VraSR mutant was more susceptible to phagocytosis by human PMNs and had greater sensitivity to oxidant and lysozyme than wild-type S. suis. Furthermore, in vitro findings and in vivo evidence from a mouse infection model together strongly demonstrate that ΔvraSR had greatly attenuated virulence compared with wild-type S. suis. Collectively, our data reveal that VraSR is a critical regulatory system that contributes to the survival of S. suis and its ability to defend against host innate immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.