Project description:Staphylococcus epidermidis is a Gram-positive, coagulase-negative (CoNS) bacterium that is carried asymptomatically on the skin and mucous membranes of virtually all human beings. It is a major cause of nosocomial infections and associated with invasive procedures (Méric et al., 2018). Virulent S. epidermidis strains contaminate indwelling medical devices, such as catheters or implants (Sabaté Brescó et al., 2017), showing pathogenicity traits, e.g., biofilm formation, cell toxicity, or methicillin resistance (Méric et al., 2018). Apart from that, even the low-virulent, low-biofilm forming strain of S. epidermidis ATCC 12228 was shown to form a biofilm under decreased oxygen conditions (Uribe-Alvarez et al., 2015). As a member of the skin and mucosal microbiome, S. epidermidis prevents the colonization of Staphylococcus aureus (Otto, 2011). Its well-studied metabolism and the ability to grow on known media make S. epidermidis a possible reconstruction candidate. A reconstruction of a genome-scale metabolic model (GEM) of S. epidermidis was created using CarveMe (Machado et al., 2018) and carefully refined in subsequent manual curation efforts, using the S. epidermidis ATCC 12228 strain sequence. The model was experimentally validated on multiple media under varying growth conditions, such as different carbon sources.
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.
Project description:We report the application of single cell RNA sequencing technology for high-throughput profiling of nasal microbiome Staphylococcus epidermidis in human nasal epithelial cells.
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.
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.
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.
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