Staphylococcus epidermidis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA382527 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5951470_1.fastq.gz | Fastqsanger.gz | |||
| SRR5951470_2.fastq.gz | Fastqsanger.gz | |||
| SRR5951480_1.fastq.gz | Fastqsanger.gz | |||
| SRR5951480_2.fastq.gz | Fastqsanger.gz | |||
| SRR5951490_1.fastq.gz | Fastqsanger.gz |
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Project description:S. aureus isolates from orthopedic device related infections
| PRJNA529795 | ENA
Project description:This study is focused on understanding the molecular basis of protein- and polysaccharide intercellular adhesin (PIA)- mediated biofilm formation by S. epidermidis in PCs. Comparative transcriptomic analysis of S. epidermidis PIA- biofilm positive (AZ22, AZ39) and PIA+ biofilm positive (ST02) strains was performed using a RNAseq approach. Pathway enrichment analysis revealed cellular component GO term (AZ22), two KEGG pathways (AZ39), and two molecular function GO term and 8 KEGG pathways (ST02) were enriched. Remarkably, glutamate biosynthesis and tricarboxylic acid cycle (TCA) genes were upregulated in AZ22 and AZ39, respectively whereas arginine deiminase (ADI) pathway genes were downregulated in ST02. Moreover, genes conferring resistance against antimicrobial peptides (AMPs) and antibiotics such as lysostaphin, fusidic acid and tetracycline were upregulated, thus implying their increased resistance in S. epidermidis grown in PCs. Notably, expression of genes conferring resistance against aminoglycoside (in AZ22) and methicillin (in AZ39 and ST02) were downregulated. This study provided an overview, how biofilm-mediated virulence, antibiotic resistance and metabolic pathways are interlinked and reprogrammed during biofilm maturation in PCs which will be intriguing in development of novel preventive strategies against S. epidermidis transfusion-transmitted infections.
2020-07-14 | GSE154352 | 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: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 among infected patients. In order to better understand the role of BRC in the pathogenesis of S. epidermidis biofilm-related infections, the transcriptome of these cells was evaluated upon exposure to human blood components. The major alterations observed were involved in the biosynthesis and metabolism of amino acids and import and export of substances through ABC transporters. In addition, the transcription of genes involved in biotin metabolism was found significantly up-regulated suggesting this pathway as a possible target for future therapeutic strategies.
2017-02-10 | GSE79948 | GEO
Project description:The custom-made S. epidermidis GeneChips(Shanghai Biochip Co., Ltd) included qualifiers representing open reading frame (ORF) sequences identified in the genomes of the S. epidermidis strain RP62A, as well as unique ORFs in S. epidermidis strain 12228. The GeneChips were composed of cDNA array containing PCR products of 2316 genes and oligonucleotide array containing 252 genes.Two-component regulatory systems (TCSs) play a pivotal role in bacterial adaptation, survival, and virulence by sensing changes in the external environment and modulating gene expression in response to a variety of stimuli.To investigate the regulatory role of LytSR, one of the TCSs identified in the genomes of S. epidermidis, we used the GeneChips to perform a transcriptional profile analysis of the wild strain and lytSR mutant.
2010-03-08 | GSE20652 | GEO
Project description:We use the zebrafish embryo model to study the innate immune response against Staphylococcus epidermidis. Therefore, we injected S. epidermidis (and three controls groups) into the yolk at 2 hpf and samples at mutiple timepoints. Gene expression profiles were obtained at 6, 30, 54, 78, 102 and 126 hpi by microarrays. The results show that the gram-positive bacterium S. epidermidis induces a late immune response with a strong response at 102 hpi.
2013-04-01 | GSE37227 | GEO
Project description:We use the zebrafish embryo model to study the innate immune response against Staphylococcus epidermidis. Therefore, we injected S. epidermidis into the yolk at 2 hpf and took samples at 5 days post injection.
2013-04-01 | GSE42846 | GEO
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:Autoinducer 2 (AI-2), a widespread by-product of the LuxS-catalyzed S-ribosylhomocysteine cleavage reaction in the activated methyl cycle, has been suggested to serve as an intra- and interspecies signaling molecule, but in many bacteria AI-2 control of gene expression is not completely understood. Particularly, we have a lack of knowledge about AI-2 signaling in the important human pathogens Staphylococcus aureus and S. epidermidis. Here, to determine the role of LuxS and AI-2 in S. epidermidis, we analyzed genome-wide changes in gene expression in an S. epidermidis luxS mutant and after addition of AI-2 synthesized by over-expressed S. epidermidis Pfs and LuxS enzymes. Genes under AI-2 control included mostly genes involved in sugar, nucleotide, amino acid, and nitrogen metabolism, but also virulence-associated genes coding for lipase and bacterial apoptosis proteins. In addition, we demonstrate by liquid chromatography/mass-spectrometry of culture filtrates that the pro-inflammatory phenol-soluble modulin (PSM) peptides, key virulence factors of S. epidermidis, are under luxS/AI-2 control. Our results provide a detailed molecular basis for the role of LuxS in S. epidermidis virulence and suggest a signaling function for AI-2 in this bacterium. Keywords: wild type without glucose control vs luxS mutant vs luxS mutant with auto-inducer II
2008-10-10 | GSE9427 | GEO
Project description:Population genomics of Staphylococcus epidermidis ST2
| PRJNA308322 | ENA