ArticleJournal of innate immunity2014
The role of innate immunity in promoting SaeR/S-mediated virulence in Staphylococcus aureus.
Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 51 citations in OpenAlex.
- GrowingInfection and immunity · 2026Article
- Candida albicans activates Staphylococcus aureus virulence regulatory systems to drive toxin-mediated human cell death.PLoS pathogens · 2026Article
- Human neutrophil α-defensin HNP1 interacts with bacterial cell wall components to promote biofilm formation byBiofilm · 2025Article
- Article
- Linking Virulence and Iron Limitation Response inJournal of proteome research · 2025Article
- Lung surfactant reducesMicrobiology spectrum · 2025Article
- Human neutrophil defensin-1 binding increases histidine kinase activity of SaeS inBiochemistry and biophysics reports · 2025Article
- Repurposing Diflunisal as an Antivirulence Agent AgainstInfectious microbes & diseases · 2025Article
- Staphylococcus aureus SaeRS impairs macrophage immune functions through bacterial clumps formation in the early stage of infection.NPJ biofilms and microbiomes · 2024Article
- The Relative Importance of Cytotoxins Produced by Methicillin-ResistantMicroorganisms · 2024Article
- Article
- SaeR as a novel target for antivirulence therapy againstEmerging microbes & infections · 2023Article
- Staphylococcus aureus SigS Induces Expression of a Regulatory Protein Pair That Modulates Its mRNA Stability.Journal of bacteriology · 2023Article
- SarS Is a Repressor of Staphylococcus aureus Bicomponent Pore-Forming Leukocidins.Infection and immunity · 2023Article
- A genetic regulatory see-saw of biofilm and virulence in MRSA pathogenesis.Frontiers in microbiology · 2023Review
- Contribution of Coagulase and Its Regulator SaeRS to Lethality of CA-MRSA 923 Bacteremia.Pathogens (Basel, Switzerland) · 2021Article
- Article
- The Accessory GeneFrontiers in microbiology · 2020Article
- The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections.Toxins · 2019Review
- Recent Advances in Anti-virulence Therapeutic Strategies With a Focus on Dismantling Bacterial Membrane Microdomains, Toxin Neutralization, Quorum-Sensing Interference and Biofilm Inhibition.Frontiers in cellular and infection microbiology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The ability of Staphylococcus aureus to infect tissues is dependent on precise control of virulence through gene-regulatory systems. While the SaeR/S two-component system has been shown to be a major regulator of S. aureus virulence, the influence of the host environment on SaeR/S-regulated genes (saeR/S targets) remains incompletely defined. Using QuantiGene 2.0 transcriptional assays, we examined expression of genes with the SaeR binding site in USA300 exposed to human and mouse neutrophils and host-derived peptides and during subcutaneous skin infection. We found that only some of the saeR/S targets, as opposed to the entire SaeR/S virulon, were activated within 5 and 10 min of interacting with human neutrophils as well as α-defensin. Furthermore, mouse neutrophils promoted transcription of saeR/S targets despite lacking α-defensin, and the murine skin environment elicited a distinctive expression profile of saeR/S targets. These findings indicate that saeR/S-mediated transcription is unique to and dependent on specific host stimuli. By using isogenic USA300ΔsaeR/S and USA300Δagr knockout strains, we also determined that SaeR/S is the major regulator of virulence factors, while Agr, a quorum-sensing two-component system, has moderate influence on transcription of the saeR/S targets under the tested physiological conditions.
Indexed as
Identifiers
What OpenQuestion holds
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.