Ontology highlight
ABSTRACT:
PROVIDER: PRJNA504381 | ENA |
REPOSITORIES: ENA
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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: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 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:Successful dissemination of resistance to oxazolidinones in multidrug-resistant Staphylococcus epidermidis clinical isolates
| PRJEB22222 | ENA
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.
2014-08-28 | E-GEOD-60834 | biostudies-arrayexpress
Project description:Draft Genome sequences of Methicillin-Resistant Staphylococcus argenteus
| PRJNA434395 | ENA
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
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
Project description:Population analysis of Pan Drug Resistant Clinical Staphylococcus epidermidis
| PRJEB12090 | ENA
Project description:Livestock-associated (LA) methicillin-resistant Staphylococcus aureus (MRSA) and strains of sequence type 398 (ST398), which first became known for its widespread colonization of pigs but are now also rapidly emerging in the number of human colonization and infections. The ability of broad host adaption in combination with a consciously evolves by acquisition of virulence gene or mobile genetic elements (MGE) have been increasingly addressed ST398 lineage a serious threat to public health. The present study was aimed to track out how the diverse ST398 lineage, which colonized or infected in a broad range of reservoirs and various geographic regions, is actually reflected in the course of virulence evolution. We therefore profiled the extracellular proteome, representing the main reservoir of virulence factors, of 30 representative clinical isolates using label-free quantitative mass spectrometry. The results show that these isolates can be divided into five distinct clusters based on their exoproteome identities and abundance signatures. The majority of proteins identified were predicted as cytoplasmic proteins showing substantial heterogeneity among our 30 investigated isolates. Only 50% of isolates their exoproteome clustering of isolates can be correlated the clustering based on genome sequences suggested that the large-scale extend of genotype changes over time. To assess the virulence and cytotoxicity of the 30 investigated isolates, we employed infection models based on Galleria mellonella and HeLa cells. The results uncovered the grouping of clinical isolates based on their virulence or cytotoxicity have apparently distinctive exoproteome signatures and particular exoproteins could play decisive roles in pathogenicity of this specific S. aureus lineage. Altogether, the combination of exoproteome and virulence analysis contribute to the comprehensive insights for the impact of genome diversity on the global production of virulence factors of this zoonotic lineage, and more importantly, our outcomes as well as our approach provided an effective pipeline to define proteomic signatures of S. aureus virulence.
2020-08-05 | PXD013951 | Pride