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Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [Spatial Transcriptomics]

ABSTRACT: We performed spatial transcriptomics to characterize wound tissue response to commensal and pathogenic staphylococcus strains. Our analysis has revealed unique epithelial responses to each strain.

ORGANISM(S): Mus musculus

PROVIDER: GSE273931 | GEO | 2025/08/02

REPOSITORIES: GEO

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Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [bulkRNA-seq]

Project description:NHEKs wounded by scratch and incubated with CM for 24 hours were evaluated by bulk RNAseq. Principal component analysis of these data revealed wounded NHEKs exposed to S. hominis products clustered close to control keratinocytes, suggesting these groups have similar transcriptomes, while the presence of S. aureus products caused variation shift in the transcriptome to result in a distinct cluster away from control. This was supported by a heatmap of differential gene expression of S. aureus and S. hominis CM treatment showing broad S. aureus-mediated suppression of genes induced by S. hominis. Conversely, upregulation of many genes by S. aureus were downregulated by S. hominis.

2025-08-02 | GSE273933 | GEO

Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [scRNA-seq]

Project description:We used single cell sequencing to examine the response of murine dorsal skin and periwound tissue to vehicle, wild type S. aureus, or S. aureus agr mutant.

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Linear peptidomimetics as potent antagonists of Staphylococcus aureus agr quorum sensing.

Project description:Staphylococcus aureus is an important pathogen causing infections in humans and animals. Increasing problems with antimicrobial resistance has prompted the development of alternative treatment strategies, including antivirulence approaches targeting virulence regulation such as the agr quorum sensing system. agr is naturally induced by cyclic auto-inducing peptides (AIPs) binding to the AgrC receptor and cyclic peptide inhibitors have been identified competing with AIP binding to AgrC. Here, we disclose that small, linear peptidomimetics can act as specific and potent inhibitors of the S. aureus agr system via intercepting AIP-AgrC signal interaction at low micromolar concentrations. The corresponding linear peptide did not have this ability. This is the first report of a linear peptide-like molecule that interferes with agr activation by competitive binding to AgrC. Prospectively, these peptidomimetics may be valuable starting scaffolds for the development of new inhibitors of staphylococcal quorum sensing and virulence gene expression.

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The quorum-sensing agr system protects Staphylococcus aureus from oxidative stress

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-20 | GSE207045 | GEO

Salicylic acid stabilizes Staphylococcus aureus biofilm by impairing the agr quorum-sensing system.

Project description:Salicylic acid (SAL) has recently been shown to induce biofilm formation in Staphylococcus aureus and to affect the expression of virulence factors. This study was aimed to investigate the effect of SAL on the regulatory agr system and its impact on S. aureus biofilm formation. The agr quorum-sensing system, which is a central regulator in S. aureus pathogenicity, plays a pivotal role in the dispersal of S. aureus mature biofilms and contributes to the creation of new colonization sites. Here, we demonstrate that SAL impairs biofilm dispersal by interfering with agr expression. As revealed by our work, protease and surfactant molecule production is diminished, and bacterial cell autolysis is also negatively affected by SAL. Furthermore, as a consequence of SAL treatment, the S. aureus biofilm matrix revealed the lack of extracellular DNA. In silico docking and simulation of molecular dynamics provided evidence for a potential interaction of AgrA and SAL, resulting in reduced activity of the agr system. In conclusion, SAL stabilized the mature S. aureus biofilms, which may prevent bacterial cell dissemination. However, it may foster the establishment of infections locally and consequently increase bacterial persistence leading to therapeutic failure.

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Single-cell approach dissecting agr quorum sensing dynamics in Staphylococcus aureus

Project description:RNAseq of exponentially growing cultures of the four agr prototype strains used in the study to investigate if differential expression of regulators interacting with the agr system could explain the differences in AIP sensitivity. Abstract Staphylococcus aureus both colonizes humans and causes severe virulent infections. Virulence is regulated by the agr quorum sensing system and its autoinducing peptide (AIP), with dynamics at the single-cell level across four agr-types – each defined by distinct AIP sequences and capable of cross-inhibition – remaining elusive. Employing microfluidics, time-lapse microscopy, and deep-learning image analysis, we uncovered significant differences in AIP sensitivity among agr-types. We observed bimodal agr activation, attributed to intergenerational phenotypic stability and influenced by AIP concentration. Upon AIP stimulation, agr III showed AIP insensitivity, while agr II exhibited increased sensitivity and prolonged generation time. Beyond expected cross-inhibition of agr I by heterologous AIP II and III, the presumably cross-activating AIP IV also inhibited agr I. Community interactions across different agr-type pairings revealed four main patterns: stable or switched dominance, and delayed or stable dual activation, influenced by community characteristics. These insights underscore the potential of personalized treatment strategies considering virulence and genetic diversity.

2024-03-05 | E-MTAB-13859 | biostudies-arrayexpress

Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [Spatial Transcriptomics]

Project description:Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [Spatial Transcriptomics]

| PRJNA1144120 | ENA

Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [scRNA-seq]

Project description:Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [scRNA-seq]

| PRJNA1144119 | ENA

Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [bulkRNA-seq]

Project description:Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [bulkRNA-seq]

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The agr quorum sensing system in Staphylococcus aureus cells mediates death of sub-population.

Project description:ObjectiveIn the human pathogen, Staphylococcus aureus, the agr quorum sensing system controls expression of a multitude of virulence factors and yet, agr negative cells frequently arise both in the laboratory and in some infections. The aim of this study was to examine the possible reasons behind this phenomenon.ResultsWe examined viability of wild type and agr mutant cell cultures using a live-dead stain and observed that in stationary phase, 3% of the wild type population became non-viable whereas for agr mutant cells non-viable cells were barely detectable. The effect appears to be mediated by RNAIII, the effector molecule of agr, as ectopic overexpression of RNAIII resulted in 60% of the population becoming non-viable. This effect was not due to toxicity from delta toxin that is encoded by the hld gene located within RNAIII as hld overexpression did not cause cell death. Importantly, lysed S. aureus cells promoted bacterial growth. Our data suggest that RNAIII mediated cell death of agr positive but not agr negative cells provides a selective advantage to the agr negative cell population and may contribute to the common appearance of agr negative cells in S. aureus populations.

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