RNA-seq Analysis of Enterococcus faecalis in Response to Surfactin Treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Enterococcus faecalis
PROVIDER: GSE280692 | GEO | 2024/11/08
REPOSITORIES: GEO
Similar Datasets
Project description:We found that biofilm formation ability of E. faecalis was impacted by culture supernatant of probiotic B. subtilis natto. To further understand how E. faecalis responded to B. subtilis natto supernatant, we searched for differentially expressed genes between E. faecalis treated with or without B. subtilis natto supernatant using RNA-seq analysis.
2021-12-29 | GSE184249 | GEO
Project description:The biofilm proteome profile of endodontic and systemic pathogen E. faecalis has been analysed in this study to identify markers associated with its biofilm formation. Strong and weak biofilm forming E. faecalis clinical isolates were compared with two standard ATCC strains of E. faecalis in order to elucidate the biological pathways associated with the biofilm formation capability of E. faecalis.
2018-01-29 | PXD006542 | Pride
Project description:Enterococcus faecalis is a major nosocomial pathogen frequently isolated from non- healing wound infections. The major factor responsible for the virulence and establishment of infection is its ability to form robust biofilm. This renders the recalcitrant nature of Enterococci towards the current treatment strategies. In the present study, the quantitative proteomic approach is carried out to elucidate the protein expression levels in E. faecalis at planktonic and biofilm stages. This will help to identify biofilm associated pathways in E. faecalis which inturn can be considered as novel targets for biofilm inhibition.
2019-07-12 | PXD010770 | Pride
Project description:Enterococcus faecalis is a common commensal organism and a prolific nosocomial pathogen that causes biofilm-associated infections. Numerous E. faecalis OG1RF genes required for biofilm formation have been identified, but few studies have compared genetic determinants of biofilm formation and biofilm morphology across multiple conditions. Here, we cultured transposon (Tn) libraries in CDC biofilm reactors in two different media and used Tn sequencing (TnSeq) to identify core and accessory biofilm determinants, including many genes that are poorly characterized or annotated as hypothetical. Multiple secondary assays (96-well plates, submerged Aclar, and MultiRep biofilm reactors) were used to validate phenotypes of new biofilm determinants.
2021-04-03 | GSE171419 | GEO
Project description:Enterococcus faecalis is a commensal bacterium in the gastrointestinal tract (GIT) of humans and other organisms. Outside of the GIT, E. faecalis can cause infections in root canals, wounds, surgical sites, the urinary tract, and on heart valves. Many of these infections can be polymicrobial, and a variety of toxins and nutritional signals influence interactions between E. faecalis and other microbes. Like other bacteria, E. faecalis metabolizes arginine through the arginine deiminase (ADI) pathway, which converts arginine to ornithine and releases ATP, ammonia, and CO2. E. faecalis arginine metabolism also affects virulence of other pathogens, such as Clostridioides difficile and Escherichia coli, during co-culture. E. faecalis may encounter elevated levels of arginine in the GIT or the oral cavity, where arginine is used as an additive in dental therapeutics to disrupt plaque formation and biofilm growth by oral streptococci. However, little is known about how E. faecalis responds to growth in arginine. To address this gap, we used RNAseq and additional in vitro assays to measure changes in growth, gene expression, and biofilm formation in arginine relative to control conditions. Here, we demonstrate that arginine decreases E. faecalis biofilm production and causes widespread differential expression of genes related to metabolism, nutrient transport, quorum sensing, and polysaccharide synthesis. Growth in arginine also increases aggregation of E. faecalis cultures and promotes decreased susceptibility to the antibiotics ampicillin and ceftriaxone. Together, this shows that E. faecalis undergoes global transcriptional changes during growth in arginine and provides a platform for better understanding of how the presence of arginine in the niches colonized by E. faecalis affects the physiology of this organism in addition to the virulence of surrounding microbes.
2024-05-28 | GSE268264 | GEO
Project description:Enterococcus faecalis is often co-isolated with Pseudomonas aeruginosa in mixed-species biofilm-associated infections of wounds and the urinary tract. As a defence strategy, the host innately restricts iron availability at infection sites. Despite their co-prevalence, the polymicrobial interactions of these two pathogens in low iron conditions, such as those found in the host, remains unexplored. Here we show that E. faecalis inhibits P. aeruginosa growth within macrocolony biofilms when iron is restricted. E. faecalis lactate dehydrogenase (ldh1) gives rise to L-lactate production during fermentative growth. We find that E. faecalis ldh1 mutant fails to inhibit P. aeruginosa growth. Additionally, we demonstrate that ldh1 expression is induced when iron is restricted, resulting in increased lactic acid exported and consequently, a reduction in pH. Together, our results suggest that E. faecalis synergistically impact P. aeruginosa growth negatively by decreasing environmental pH and L-lactate-mediated iron chelation. Overall, this study highlights that the microenvironment in which the infection occurs is important for understanding its pathophysiology.
2022-06-15 | GSE190090 | GEO
Project description:Transcriptional profiling of E. faecalis E99 WT and an isogenic ΔperA strain grown in THB + 1% glucose. Pathogenic E. faecalis are enriched for a pathogenicity island (PAI). This 150-kb island harbors a number of well characterized virulence genes plus a number of determinants of unknown function including one encoding a transcriptional regulator, designated PerA. In this work, we show that PerA coordinately regulates both metabolic and virulence genes, and influences the platelet binding ability of E. faecalis. Finally, we show that PerA responds to bicarbonate, an intestinal ion frequently used by pathogens to determine the site of infection. Together, these results indicate that PerA is a global transcriptional regulator that coordinately regulates genes responsible for enterococcal pathogenicity. These findings highlight a novel feature of PAI-mediated virulence regulation, namely the coordinate regulation of metabolic and virulence factors in the core genome by a horizontally acquired PAI-encoded transcriptional regulator.
2012-08-16 | GSE31538 | GEO
Project description:Transcriptional profiling of E. faecalis E99 WT and an isogenic ΔperA strain grown in THB + 1% glucose. Pathogenic E. faecalis are enriched for a pathogenicity island (PAI). This 150-kb island harbors a number of well characterized virulence genes plus a number of determinants of unknown function including one encoding a transcriptional regulator, designated PerA. In this work, we show that PerA coordinately regulates both metabolic and virulence genes, and influences the platelet binding ability of E. faecalis. Finally, we show that PerA responds to bicarbonate, an intestinal ion frequently used by pathogens to determine the site of infection. Together, these results indicate that PerA is a global transcriptional regulator that coordinately regulates genes responsible for enterococcal pathogenicity. These findings highlight a novel feature of PAI-mediated virulence regulation, namely the coordinate regulation of metabolic and virulence factors in the core genome by a horizontally acquired PAI-encoded transcriptional regulator. RNA was obtained from E. faecalis E99 ΔperA from mid-log (OD600 0.05), late log (OD600 0.5) and stationary phase (OD600 1.0) and compared to E. faecalis E99 WT RNA extracted from the same growth phases. Cultures were grown in THB + 1% glucose.
2012-08-16 | E-GEOD-31538 | biostudies-arrayexpress
Project description:Transcriptional profiling to investigate the effect of drug treatment on the E. faecalis cells. For microarray analysis, E. faecalis OG1RF was grown in FMC medium supplemented with 10 mM glucose to an optical density at 600 nm (OD600) of 0.3 and the cultures were divided in 3 aliquots. One aliquot was collected by centrifugation and immediately frozen (untreated control cells). The other aliquots were treated for 30 or 60 min with 1.25 X the minimum inhibitory concentration (MIC) of vancomycin (10 μg ml-1). After an exposure time of 30 or 60 minutes, each of these cultures was also centrifuged and the pellets frozen. RNA was then isolated from each pellet for microarray analysis. This process was repeated 3 additional times, for a total of four replicates of each condition.
2013-03-19 | GSE45300 | GEO
Project description:Enterococcus faecalis is a natural inhabitant of the human gastrointestinal tract. In a healthy physiological state of the gut (eubiosis), E. faecalis is a subdominant species in the intestinal microbiota. When the intestinal homeostasis is disrupted (dysbiosis), it becomes dominant species and can cause infections. The prominence of bile acids deoxycholate (DCA) hallmarks eubiosis. This experiment aimed to better understand how E. faecalis adapts to DCA. We showed that DCA impairs E. faecalis growth and imposes permanent adjustments to the expression of many crucial genes, including a majority of factors enabling translation. Thus, the drastic decrease of DCA amounts during dysbiosis may account for the rise of E. faecalis population.
2022-05-20 | GSE192438 | GEO