Linezolid resistant Staphylococcus epidermidis
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB22222 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2117830_1.fastq.gz | Fastqsanger.gz | |||
| ERR2117830_2.fastq.gz | Fastqsanger.gz | |||
| ERR2117840_1.fastq.gz | Fastqsanger.gz | |||
| ERR2117840_2.fastq.gz | Fastqsanger.gz | |||
| ERR2117850_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:The release of cells from S. epidermidis biofilms formed on medical devices has been associated with the onset of bloodstream infections, resulting in increased morbidity and mortality rates. This has to do, in part, with the difficulty to accurately diagnose S. epidermidis bloodstream infections. S. epidermidis is a ubiquitous commensal of human skin and mucosa and, thus, a positive blood culture does not always represent an infection, possibly being the result of contamination during blood collection. As such, there is a high demand to find markers that can help clinicians to distinguish infection (clinical isolates) from contamination (commensal strains). With that in mind, several studies comparing phenotypic or genetic characteristics of clinical and commensal isolates have been performed over the years. However, because S. epidermidis virulence factors seem to be the same that confer its fitness as a commensal, we hypothesized that the ability of S. epidermidis strains to adapt to the host environment may not depend on a specific phenotypic and/or genetic makeup, but rather on the regulation of gene transcription. Thus, using RNA-Sequencing (RNA-seq), we characterized the transcriptome of commensal and clinical isolates in the context of infection to try to uncover differences and, thus, identify markers that could be used for the diagnostics. Several markers with the potential to discriminate between both groups were highlighted. Nevertheless, when the results obtained were confirmed in a wider collection of clinical and commensal isolates the discriminatory power of the genes initially identified was lost. Although we cannot rule out that the characterization of a larger collection of isolates would identify potential candidates, our transcriptomic data was not able to confirm our initial hypothesis, evidencing S. epidermidis opportunistic nature.
2022-12-09 | GSE179407 | GEO
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
2017-01-06 | GSE85265 | GEO
Project description:To explain enhanced biofilm formation and increased dissemination of S. epidermidis in mixed-species biofilms, microarrays were used to explore differential gene expression of S. epidermidis in mixed-species biofilms. One sample from single species biofilm (S1) and mixed-species biofilm (SC2) were excluded from analyses for outliers. We observed upregulation (2.7%) and down regulation (6%) of S. epidermidis genes in mixed-species biofilms. Autolysis repressors lrgA and lrgB were down regulated 36-fold and 27-fold respectively and was associated with increased eDNA possibly due to enhanced autolysis in mixed-species biofilms. These data suggest that bacterial autolysis and release of eDNA in the biofilm matrix may be responsible for enhancement and dissemination of mixed-species biofilms of S. epidermidis and C. albicans.
2012-02-28 | GSE35438 | GEO
Project description:To explain enhanced biofilm formation and increased dissemination of S. epidermidis in mixed-species biofilms, microarrays were used to explore differential gene expression of S. epidermidis in mixed-species biofilms. One sample from single species biofilm (S1) and mixed-species biofilm (SC2) were excluded from analyses for outliers. We observed upregulation (2.7%) and down regulation (6%) of S. epidermidis genes in mixed-species biofilms. Autolysis repressors lrgA and lrgB were down regulated 36-fold and 27-fold respectively and was associated with increased eDNA possibly due to enhanced autolysis in mixed-species biofilms. These data suggest that bacterial autolysis and release of eDNA in the biofilm matrix may be responsible for enhancement and dissemination of mixed-species biofilms of S. epidermidis and C. albicans. Staphylococcal gene expression in mixed-species biofilms with Candida and in single species biofilms of S. epidermidis were analyzed. The experiment was repeated thrice on 3 different days (3 biological replicates each for single species biofilms of S. epidermidis and mixed-species biofilms). Only 2 biological replicates were analyzed and one biological replicate was not analyzed (S1 and SC1 - raw data files are provided on the Series record). Single species biofilms of S. epidermidis (strain 1457) and C. albicans (strain 32354) and mixed-species biofilms were formed on 6-well tissue culture plates. Five ml of organism suspensions (O.D. 0.3, S. epidermidis 107 CFU/ml or C. albicans 105 CFU/ml) or 2.5 ml each for mixed-species biofilms for 24 hr. RNA was harvested from single species and mixed-species biofilms.
2012-02-28 | E-GEOD-35438 | biostudies-arrayexpress
Project description: Not available
| S-EPMC4012793 | biostudies-literature
Project description:We performed differential RNA-seq of two Staphylococcus epidermidis clinical isolates (PS2 and PS10) to compare their transcription profiles. The isolates were originally obtained from blood cultures during a systemic infection in an immunocompromised patient (Weisser et al. 2010. J Clin Microbiol 48: 2407-2412). They are of clonal origin, but differ phenotypically with respect to extracellular biofilm matrix production. Thus PS2, isolated in the early stage of the infection, forms a weak biofilm mediated by protein-protein interactions, while PS10, which was obtained at the end of the infection course, forms a strong biofilm through production of a polysaccharide intercellular adhesin (PIA) extracellular biofilm matrix. Transcription profiling by dRNA-seq was performed to elucidate differentially expressed metabolic pathways and regulators contributing to the switch in extracellular biofilm matrix producction between the two isolates.
2019-02-05 | GSE126097 | GEO
Project description:The ability of S. epidermidis to withstand the high bactericidal activity of the host’s blood is crucial for its systemic dissemination. Hence, in order to identify genes and pathways involved in the bacterium’s survival in human blood, we have characterized the transcriptome of S. epidermidis biofilms upon contact with human blood. Our results showed that genes whose transcription was increased in blood included those involved in biosynthesis and metabolism of amino acids, small molecules, carboxylic and organic acids, and cellular ketones. One of the striking changes, observed after 4 hours of exposure to human blood, was the increase in the expression of genes involved in iron utilization, suggesting iron acquisition is an important component of S. epidermidis survival in human blood.
2014-08-29 | GSE52111 | GEO
Project description:We report on an analysis of sequential isolates of Staphylococcus epidermidis from cultures of blood obtained from a patient with acute myeloid leukemia while the patient was receiving linezolid treatment. All 12 isolates had a linezolid MIC of 32 microg/ml. A 420-bp domain V region of the 23S rRNA gene from all isolates was amplified, and their nucleotide sequences were determined. A G2576T mutation was identified in all isolates. It was estimated that 67% of the 23S rRNA genes carried this mutation. This is the first report of the failure of linezolid treatment for Staphylococcus epidermidis bacteremia associated with a G2576T mutation in an immunocompromised patient.
| S-EPMC2045370 | biostudies-literature
Project description:The ability of S. epidermidis to withstand the high bactericidal activity of the hostM-bM-^@M-^Ys blood is crucial for its systemic dissemination. Hence, in order to identify genes and pathways involved in the bacteriumM-bM-^@M-^Ys survival in human blood, we have characterized the transcriptome of S. epidermidis biofilms upon contact with human blood. Our results showed that genes whose transcription was increased in blood included those involved in biosynthesis and metabolism of amino acids, small molecules, carboxylic and organic acids, and cellular ketones. One of the striking changes, observed after 4 hours of exposure to human blood, was the increase in the expression of genes involved in iron utilization, suggesting iron acquisition is an important component of S. epidermidis survival in human blood. Twenty-four hour S. epidermidis biofilms were incubated with either whole human blood or tryptic soy broth (TSB) during 2 or 4 hours at 37oC, 5% CO2 and slight agitation. RNA was then extracted and the transcriptomic libraries constructed. Differential gene expression calculations were performed using the transcriptome of biofilms at the start of the culture (T0h) as a control. This experiment was performed twice with blood collected from 6 healthy human donors under a protocol approved by the PartnerM-bM-^@M-^Ys Health Care System Institutional Review Board (Boston, MA, USA).
2014-08-29 | E-GEOD-52111 | biostudies-arrayexpress
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