Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pseudomonas aeruginosa

ABSTRACT: Whole-genome sequencing of Pseudomonas aeruginosa from newly-infected individuals with cystic fibrosis

PROVIDER: PRJNA875460 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR21391400_1.fastq.gz	Fastqsanger.gz
	SRR21391400_2.fastq.gz	Fastqsanger.gz
	SRR21391500_1.fastq.gz	Fastqsanger.gz
	SRR21391500_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 1165

Similar Datasets

Transcription profiling by array of Pseudomonas aeruginosa wild-type and phhR mutants grown in a defined synthetic cystic fibrosis sputum medium with and without aromatic amino acids

Project description:Arrays comparing Pseudomonas aeruginosa growth in a defined synthetic cystic fibrosis sputum medium with and without aromatic amino acids. Additional arrays comparing wild-type Pseudomonas aeruginosa and phhR mutant P. aeruginosa in defined synthetic cystic fibrosis sputum medium.

2010-04-01 | E-MEXP-2593 | biostudies-arrayexpress

Novel virulence factors in host-adapted Pseudomonas aeruginosa infection of the Cystic Fibrosis airways

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

2010-11-04 | E-GEOD-25130 | biostudies-arrayexpress

Transcription profiling of Pseudomonas aeruginosa PA14 grown in aerobic or anaerobic conditions in cystic fibrosis sputum with added nitrate

Project description:Effect of anaerobic growth condition on gene expression profile of Pseudomonas aeruginosa PA14 grown in cystic fibrosis sputum with 100 mM nitrate added

2007-06-01 | E-MEXP-1051 | biostudies-arrayexpress

Gene expression analysis of Pseudomonas aeruginosa wild type, delta-gbdR, and delta-plcHR deletion mutants

Project description:Pseudomonas aeruginosa is a virulent opportunistic pathogen responsible for high morbity in COPD, burns , implanted medical devices and cystic fibrosis. Pseudomonas aeruginosa is a problematic colonizer of the human lung. P. aeruginosa produces a phospholipase C (PlcH) that degrades choline-containing lipids such as phosphatidylcholine and sphingomylein that are found in lung surfactant and in host membranes. In this study, we analyzed gene expression in mutants defective in PlcH production (delta-plcH and delta-gbdR) and the wild type when growing in medium with lung surfactant.

2013-01-01 | GSE41926 | GEO

Aspergillus fumigatus transcriptome during growth in SDB, SCFM2, and co-culture with Pseudomonas aeruginosa PA14

Project description:This study examines transcriptional changes in Aspergillus fumigatus across different growth environments and in response to bacterial co-culture. A. fumigatus was grown in Sabouraud Dextrose Broth (SDB), synthetic cystic fibrosis medium 2 (SCFM2), and in co-culture with Pseudomonas aeruginosa in SCFM2. Experimental conditions include A. fumigatus monoculture in SDB, monoculture in SCFM2, and co-culture with P. aeruginosa in SCFM2, each performed in biological triplicate. Total RNA was extracted from cultures and rRNA-depleted prior to library preparation and sequencing. This dataset enables analysis of fungal transcriptional adaptation to cystic fibrosis-relevant media and identification of gene expression change associated with bacterial interaction.

2026-06-01 | E-MTAB-16731 | biostudies-arrayexpress

Gene expression in COPD and non-diseased nasopharyngeal organoids following Pseudomonas aeruginosa infection

Project description:Pseudomonas aeruginosa is a common bacteria leading to exacerbations of chronic obstructive pulmonary disease (COPD) patients while this bacteria can be easily eradicated by the immune systems of healthy individuals. Human airway organoids derived from healthy individuals and COPD patients were infected with pseudomonas aeruginosa. This project aims (1) to understand the differences in gene expressions in healthy and COPD airway organoids during stable condition, without infection and (2) to investigate differential pathogenic mechanism (i.e. antimicrobial defense) of pseudomonoas aeruginosa infection in healthy and COPD populations. Three healthy donors and three COPD patients were included in this study and samples were collected with and without pseudomonas aeruginosa infection.

2022-11-10 | GSE201465 | GEO

Pseudomonas aeruginosa lasR mutants in young cystic fibrosis patients

Project description:Pseudomonas aeruginosa undergoes genetic change during chronic infection of the airways of cystic fibrosis (CF) patients. One common change is mutation of lasR. LasR is a transcriptional regulator that responds to one of the quorum sensing signals in P. aeruginosa, and regulates acute virulence factor expression as well as central metabolic functions. P. aeruginosa mutants in which lasR was inactivated emerged in the airways of CF patients early during chronic infection, and during growth in the laboratory on Luria-Bertani agar. Both environments are rich in amino acids. Inactivation of lasR in these isolates conferred a growth advantage with amino acids, a phenotype that could account for selection of lasR mutants both in vivo and in vitro. P. aeruginosa lasR mutants were identified by their distinctive colony morphology, including autolysis that correlated with an imbalance in 4-hydroxy-2-alkylquinolines (HAQs), and an iridescent metallic sheen likely caused by the accumulation of one such HAQ. The alterations in transcriptional profile due to inactivation of lasR were conserved in isolates from multiple young CF patients. P. aeruginosa lasR mutations may represent surrogate markers to delineate stages in the natural history of CF airway disease, each with different prognostic and therapeutic implications, analogous to the markers used to direct cancer treatment. Similar to cancer cell mutations that promote unrestricted growth, lasR mutations may promote unrestricted growth of P. aeruginosa in the CF airway by enabling more efficient utilization of available amino acids. Analyse the effects of mutation of the lasR gene in Pseudomonas aeruginosa isolates from cystic fibrosis patients by comparing the transcriptional profile of an isolate from a young patient with that of an isogenic engineered lasR mutant.

2010-06-30 | E-GEOD-5560 | biostudies-arrayexpress

Transcription profiling of Dictyostelium discoideum in response to infection with Pseudomonas aeruginosa PA01 and PA14 strains which differ in virulence

Project description:Pseudomonas aeruginosa is an opportunistic human pathogen, infecting immuno-compromised patients and causing persistent respiratory infections in people affected from cystic fibrosis. Pseudomonas strain Pseudomonas aeruginosa PA14 shows higher virulence than Pseudomonas aeruginosa PAO1 in a wide range of hosts including insects, nematodes and plants but the precise cause of this difference is not fully understood. Little is known about the host response upon infection with Pseudomonas and whether or not transcription is being affected as a host defense mechanism or altered in the benefit of the pathogen. In this context the social amoeba Dictyostelium discoideum has been described as a suitable host to study virulence of Pseudomonas and other opportunistic pathogens.

2008-07-09 | E-TABM-464 | biostudies-arrayexpress

High-throughput 3-prime end RNA-seq of Pseudomonas aeruginosa response to Azithromycin

Project description:P. aeruginosa produces serious chronic infections in hospitalized patients and immunocompromised individuals, including cystic fibrosis patients. The molecular mechanisms by which P. aeruginosa responds to antibiotics and other stresses to promote persistent infections may provide new avenues for therapeutic intervention. Azithromycin (AZM), an antibiotic frequently utilized in cystic fibrosis treatment, is thought to improve clinical outcomes through a number of mechanisms including impaired biofilm growth and quorum sensing in P. aeruginosa. However, the mechanisms underlying the transcriptional response to AZM remain unclear. Here, we interrogated the P. aeruginosa transcriptional response to AZM using a fast and affordable genome-wide approach to quantitate RNA 3-prime-ends (3pMap). We identify new riboregulators and identify a prominent role of transcription termination in the response to AZM treatment.

2021-06-08 | GSE173073 | GEO

Pseudomonas aeruginosa cystic fibrosis strains share a core proteome

Project description:The opportunistic pathogen Pseudomonas aeruginosa is among the main colonizers of the lungs of cystic fibrosis (CF) patients. We have isolated and sequenced several P. aeruginosa isolates from the sputum of CF patients and used phenotypic, genomic and proteomic analyses to compare these CF derived strains with each other and with the model strain PAO1.

2015-10-14 | PXD002865 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data