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Staphylococcus epidermidis strain:1585 | isolate:1585

ABSTRACT: Staphylococcus epidermidis strain:1585 | isolate:1585 Genome sequencing

PROVIDER: PRJNA1068359 | ENA |

REPOSITORIES: ENA

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Proteomic analysis of a commensal Staphylococcus epidermidis strain in different pH conditions.

Project description:Proteomic analysis of a commensal Staphylococcus epidermidis strain in different pH conditions for describing the molecular players involved in the skin-to-blood adaptation of the bacterium.

2023-03-11 | PXD034825 | Pride

Dual effect of Staphylococcus epidermidis DnaK on Staphylococcus aureus biofilm proteostasis and regulation

Project description:Staphylococcus aureus and Staphylococcus epidermidis, two Gram-positive bacteria commonly found in the human skin microbiota, form biofilms that contribute to skin dysbiosis and play a key role in conditions like acne and atopic dermatitis. The Calcitonin Gene-Related Peptide (CGRP) is a human peptide involved in skin inflammation. We previously showed that CGRP enhances the virulence of S. epidermidis MFP04 and that the DnaK chaperone protein is significantly overexpressed in the secretome of CGRP-activated virulent S. epidermidis. In this study, we explored a potential new role of S. epidermidis DnaK in biofilm formation in both S. aureus and S. epidermidis. We showed that recombinant S. epidermidis DnaK differentially affects biofilm formation, whether in two skin commensal staphylococcal strains (S. aureus MFP03 and S. epidermidis MFP04) or in a clinical S. aureus strain (CIP 107093). In the clinical strain S. aureus CIP 107093, biofilm formation was most strongly inhibited. This inhibition involves both the Substrate-Binding Domain and the Nucleotide-Binding Domain of DnaK. Proteomic analysis revealed that DnaK alters the S. aureus biofilm proteome, stabilizing proteins involved in protein degradation like ClpP and ETA, while downregulating key regulatory proteins involved in biofilm development such as SaeS and WalK. These results indicate that S. epidermidis DnaK may contribute to the regulation of S. aureus biofilm formation, suggesting a cross-species regulatory role of DnaK within the skin microbiota.

2026-03-09 | PXD062742 | Pride

Dormancy within Staphylococcus epidermidis biofilms: a transcriptomic analysis by RNA-seq

Project description:We sequenced mRNA from three independent biological replicates of Staphylococcus epidermidis biofilms with different proportion of dormant cells. Whole trancriptome analysis of Staphylococcus epidermidis biofilms with prevented and induced dormancy.

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Staphylococcus aureus and Staphylococcus epidermidis transcriptomic response to sapienic acid

Project description:Staphylococcus aureus Newman and Staphylococcus epidermidis Tu3298, 20 minutes post challenge with sub-inhibitory concentration of sapienic acid vs equivalent concentration of ethanol. Challenge was added at mid logarithmic growth (OD600 0.5). Biological triplicates of samples were sequenced.

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Project description:We examined the differential gene expression of Staphylococcus epidermidis and Staphylococcus epidermidis in dual species biofilms. Therefore, we performed RNA-Seq on single and dual species biofilms and we compared the gene expression levels in dual species biofilms to those in single species biofilms.

2016-05-27 | GSE79575 | GEO

Toxin mediates sepsis caused by methicillin-resistant Staphylococcus epidermidis

Project description:Bacterial sepsis is a major killer in hospitalized patients. Coagulase-negative staphylococci (CNS) with the leading species Staphylococcus epidermidis are the most frequent causes of nosocomial sepsis, with most infectious isolates being methicillin resistant. However, which bacterial factors underlie the pathogenesis of CNS sepsis is unknown. While it has been commonly believed that invariant structures on the surface of CNS trigger sepsis by causing an over-reaction of the immune system, we show here that sepsis caused my methicillin-resistant S. epidermidis is to a large extent mediated by the methicillin resistance island-encoded peptide toxin, PSM-mec. PSM-mec contributed to bacterial survival in whole human blood and resistance to neutrophil-mediated killing, and caused significantly increased mortality and cytokine expression in a mouse sepsis model. Furthermore, we show that the PSM-mec peptide itself, rather than the regulatory RNA in which its gene is embedded, is responsible for the observed virulence phenotype. While toxins have never been clearly indicated in CNS infections, our study shows that an important type of infection caused by the predominant CNS species, S. epidermidis, is mediated to a large extent by a toxin. Of note, these findings suggest that CNS infections may be amenable to virulence-targeted drug development approaches. We used microarrays to detail the global gene expression between S. epidermidis strain Rp62A and S. epidermidis strain Rp62A isogenic Δpsm-mec deletion mutants

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Marker gene discovery for Staphylococcus epidermidis infection in zebrafish embryos (RNA-Seq)

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Staphylococcus epidermidis: wild type vs lytSR mutant

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Project description:Staphylococcus epidermidis strain:SEPI147 | isolate:SEPI147 Genome sequencing

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Staphylococcus epidermidis strain:SEPI148 | isolate:SEPI148

Project description:Staphylococcus epidermidis strain:SEPI148 | isolate:SEPI148 Genome sequencing

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