Pseudomonas aeruginosa
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ABSTRACT:
PROVIDER: PRJNA818324 | ENA |
REPOSITORIES: ENA
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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
Project description:Pseudomonas aeruginosa is an environmentally resilient bacterium and an important cause of both acute and chronic infections in people with impaired natural barriers or immunological defences. Chronic respiratory infection with P. aeruginosa is a major cause of morbidity and mortality in people with airway diseases, including cystic fibrosis and bronchiectasis. Chronic airway infection is characterised by periods of relative stability punctuated by pulmonary exacerbations, during which times rapid bacterial outgrowth necessitates intense antimicrobial chemotherapy. The periods of stable infection can be modelled in mice, by nasal instillation of airway-adapted P. aeruginosa in saline, leading to prolonged colonisation of both upper airway (sinus) and lower airway (lung) environments that is not associated with symptomatic disease. Here, we use NMR metabolomics to investigate the impact of P. aeruginosa colonisation on the metabolic landscape of sinuses and lungs. Lung infection led to pronounced changes in the airway metabolome, with depletion of glucose and myo-inositol but enrichment of glutathione, relative to uninfected lungs. Changes in the sinuses were more subtle but could be identified through dimensionality reduction approaches. The NMR spectral peaks which discriminated between infected and uninfected sinuses in partial least squares discriminant analysis included those for lactate and choline but were mostly representative of yet unidentified metabolites. These data highlight the differential impact of infection on separate airway compartments and identify undefined metabolites undergoing pronounced abundance changes during infection.
2025-11-06 | MTBLS6052 | MetaboLights
Project description:Chronic lung infections and presistent inflammation are a leading cause of morbidity and mortality in people with cystic fibrosis and therefore there is a need for therapies that can simultaneously eliminate infection and the hyperinflammatory lung environment in CF. Mesenchymal stromal cell-derived extracellular vesicles (MSC EVs) represent a promising solution, offering potent anti-inflammatory, immunomodulatory, and antimicrobial properties while being safe and non-toxic. This study demonstrates the efficacy of MSC EVs in a CF mouse model of acute Pseudomonas aeruginosa lung infection. MSC EVs reduced Pseudomonas burden, immune cell infiltration, and pro-inflammatory cytokine levels in the lungs.
2025-06-30 | GSE290294 | GEO
Project description:Using genome sequencing of Pseudomonas aeruginosa from non-cystic bronchiectasis lung infections
| PRJEB14952 | ENA
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
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
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
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. Pseudomonas aeruginosa was cultured in liquid cultures with aeration in a defined medium with Survanta, a lung surfactant replacement. Cultures were harvested during mid-exponential phase, and RNA was isolated for microarray analysis. The P. aeruginosa strain PAO1 wild type gene expression was compared to expression profiles from delta-gbdR and delta-plcHR deletion mutants, two mutants defective in PlcH production.
2013-01-01 | E-GEOD-41926 | biostudies-arrayexpress
Project description:Gene expression data from Pseudomonas aeruginosa strains isolated from cystic fibrosis lung infections
| PRJNA142761 | ENA
Project description:Pseudomonas aeruginosa (P. aeruginosa) lung infection is a significant cause of mortality in patients with cystic fibrosis (CF). Most CF patients acquire unique P. aeruginosa strains from the environment; however clonal strains have been identified in CF communities in several countries. Two clonal strains infect 10% to 40% of patients in three CF clinics in mainland eastern Australia. The expression profiles of four planktonically-grown isolates of one Australian clonal strain (AES-2), and four non–clonal CF P. aeruginosa isolates were compared to each other and to the reference strain PAO1 using the Affymetrix P. aeruginosa PAO1 genome array, to gain insight into properties mediating the enhanced infectivity of AES-1. The isolates were subsequently grown as 3-day old biofilms and similarly extracted for RNA and compared as above. Data analysis was carried out using BIOCONDUCTOR software. Keywords: Comparative strain hybridization
2009-02-05 | GSE10304 | GEO