Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1167871 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR30858516_1.fastq.gz | Fastqsanger.gz | |||
| SRR30858516_2.fastq.gz | Fastqsanger.gz | |||
| SRR30858517_1.fastq.gz | Fastqsanger.gz | |||
| SRR30858517_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
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Project description:Multi drug resistant Pseudomonas aeruginosa
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Project description:Pseudomonas aeruginosa chronically colonizes the lungs of individuals with CF, where it reaches high cell densities and produces a battery of virulence factors. Upon infection, a single strain of P. aeruginosa can colonize an individual’s lungs throughout his or her lifetime. To understand the evolution of P. aeruginosa during chronic lung infection, we conducted both genotypic and phenotypic analyses on clinical isogenic strains obtained from the lungs of three different individuals with CF. These strains were isolated over a period of approximately ten years and possess phenotypes that are commonly observed in isolates from the CF lung, such as the antibiotic resistant dwarf and mucoid phenotypes. Microarray analyses were carried out on isolates grown in a chemically defined medium that mimics the nutritional environment of the CF lung, synthetic CF sputum medium (SCFM).
2010-05-25 | GSE21966 | GEO
Project description:Antimicrobial peptides (AMPs) are garnering attention as possible alternatives to antibiotics. Here, we describe the antimicrobial properties of epinecidin-1 against multi-drug resistant clinical isolates of P. aeruginosa (P. aeruginosa (R)) and P. aeruginosa from ATCC (P. aeruginosa (19660)) in vivo. The minimum inhibitory concentrations (MICs) of epinecidin-1 against P. aeruginosa (R) and P. aeruginosa (19660) were determined, and compared with those of imipenem. Epinecidin-1 was found to be highly effective at combating peritonitis infection caused by P. aeruginosa (R) or P. aeruginosa (19660) in mouse models, without inducing adverse behavioral effects, or liver or kidney toxicity. Taken together, our results indicate that epinecidin-1 enhances the survival rate of mice infected with the bacterial pathogen P. aeruginosa through both antimicrobial and immunomodulatory effects. RNA from mice treated with epinecidin-1 were individually compared to RNA from PBS control mice.
2014-05-27 | E-GEOD-57976 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa chronically colonizes the lungs of individuals with CF, where it reaches high cell densities and produces a battery of virulence factors. Upon infection, a single strain of P. aeruginosa can colonize an individualâs lungs throughout his or her lifetime. To understand the evolution of P. aeruginosa during chronic lung infection, we conducted both genotypic and phenotypic analyses on clinical isogenic strains obtained from the lungs of three different individuals with CF. These strains were isolated over a period of approximately ten years and possess phenotypes that are commonly observed in isolates from the CF lung, such as the antibiotic resistant dwarf and mucoid phenotypes. Microarray analyses were carried out on isolates grown in a chemically defined medium that mimics the nutritional environment of the CF lung, synthetic CF sputum medium (SCFM). 17 clinically isolated P. aeruginosa strains from three individuals with CF (5 strains from individual P1, 7 strains from individual P2, 5 strains from individual P3). Two reference strains PAO1 and PA14. All experiments were biologically duplicated.
2010-06-08 | E-GEOD-21966 | biostudies-arrayexpress
Project description:Antimicrobial peptides (AMPs) are garnering attention as possible alternatives to antibiotics. Here, we describe the antimicrobial properties of epinecidin-1 against multi-drug resistant clinical isolates of P. aeruginosa (P. aeruginosa (R)) and P. aeruginosa from ATCC (P. aeruginosa (19660)) in vivo. The minimum inhibitory concentrations (MICs) of epinecidin-1 against P. aeruginosa (R) and P. aeruginosa (19660) were determined, and compared with those of imipenem. Epinecidin-1 was found to be highly effective at combating peritonitis infection caused by P. aeruginosa (R) or P. aeruginosa (19660) in mouse models, without inducing adverse behavioral effects, or liver or kidney toxicity. Taken together, our results indicate that epinecidin-1 enhances the survival rate of mice infected with the bacterial pathogen P. aeruginosa through both antimicrobial and immunomodulatory effects.
2014-05-27 | GSE57976 | GEO
Project description:The widespread presence of antibiotic-resistant bacteria in the environment has been recognized as an important emerging environmental contaminant. Hospital wards, as a special public indoor environment, are of great concern for the risks associated with this emerging environmental contaminant. Pseudomonas aeruginosa, a common nosocomial bacterium, is a contamination risk in the hospital environment due to its drug resistance and transmission of virulence factors. Notably, the antimicrobial peptide-sensing two-component system (TCS) ParRS and CprRS have been implicated in dynorphin-induced signaling, but the underlying Manuscript2 mechanism has remained elusive. In this study, we performed proteomic analysis to systematically investigate the contributions of ParRS and CprRS to P. aeruginosa pathogenesis and dynorphin-induced resistance to polymyxins. Additionally, we characterized the significance of the extracellular sensor domains of ParS and CprS in dynorphin perception. Furthermore, through structural biology, we identified additional TCS sensors with similar extracellular domain conformations, which also directly interacted with dynorphin in vitro. This suggests convergent evolution in different bacterial TCSs for host-derived synthetic peptide signal transmitting. Our findings establish a link between CAMPs resistance associated TCSs and virulence regulation of common nosocomial bacteria. This further illustrates the danger of this emerging contaminant for the environment and humans.
2024-07-04 | PXD043746 | Pride
Project description:The gene encoding elongation factor G, fusA1, is frequently mutated in clinical isolates of Pseudomonas aeruginosa from patients with cystic fibrosis. Recent work has shown that fusA1 mutants often display elevated aminoglycoside resistance due to increased expression of the aminoglycoside efflux pump, MexXY. We isolated a spontaneous gentamicin-resistant fusA1 mutant (FusA1-P443L) in which mexXY expression was increased. We compared the transcriptome of this fusA1 mutant (EMC1) with the P. aeruginosa PAO1-derived progenitor strain (EMC0) and complemented mutant strain expressing the wild-type fusA1 gene in trans (EMC1*).
2020-09-16 | E-MTAB-8690 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa is a predominant pathogen in chronic lung infections in individuals with cystic fibrosis (CF). Epidemic strains of P. aeruginosa, such as the Liverpool Epidemic Strain (LES), are capable of transferring between CF patients and have been associated with increased hospital visits and antibiotic treatments. Comparative genomics and phenotypic assays have shown that antibiotic resistance profiles differ among LES isolates and that genotype–phenotype associations are difficult to establish for resistance phenotypes in clinical isolates of P. aeruginosa based on these comparisons alone. We compared two LES isolates, LESlike1 and LESB58, and the common laboratory strain P. aeruginosa PAO1 using label-free quantitative proteomics to more accurately predict functional differences between strains. The proteomes of the LES isolates were found to be more similar to each other than to PAO1. However, we also observed a number of differences in the abundance of proteins involved in quorum sensing, virulence, and antibiotic resistance, including in the comparison of LESlike1 and LESB58. Specifically, the proteomic data revealed a higher abundance of proteins involved in polymyxin and aminoglycoside resistance in LESlike1. Minimum inhibitory concentration assays confirmed that LESlike1 has higher resistance to antibiotics from these classes. These findings provide an example of the ability of proteomic data to complement genotypic and phenotypic studies to understand resistance in clinical isolates.
2022-05-09 | PXD025827 | Pride
Project description:Pseudomonas aeruginosa airway infection is the primary cause of death in Cystic Fibrosis (CF). During early infection P. aeruginosa produces multiple virulence factors, which cause acute pulmonary disease and are largely regulated by quorum sensing (QS) intercellular signalling networks. Longitudinal clinical studies have observed the loss, through adaptive mutation, of QS and QS-related virulence in late chronic infection. Although the mechanisms are not understood, infection with QS mutants has been linked to a worse outcome for CF patients. By comparing QS-active and QS-inactive P. aeruginosa CF isolates, we have identified novel virulence factors and pathways associated with QS disruption. In particular, we noted factors implicating increased intra-phagocyte survival. Our data present novel targets as candidates for future CF therapies. Some of these targets are already the subject of drug development programmes for the treatment of other bacterial pathogens and may provide cross-over benefit to the CF population. Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE25128: Gene expression data from Pseudomonas aeruginosa strains isolated from cystic fibrosis lung infections GSE25129: Comparative genomic hybridisation data from Pseudomonas aeruginosa strains isolated from cystic fibrosis lung infections
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