Gene expression analysis of Pseudomonas aeruginosa wild type, delta-gbdR, and delta-plcHR deletion mutants
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ABSTRACT:
ORGANISM(S): Pseudomonas aeruginosa Pseudomonas aeruginosa PAO1
PROVIDER: GSE41926 | GEO | 2013/01/01
SECONDARY ACCESSION(S): PRJNA178535
REPOSITORIES: GEO
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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:The interactions between Gram-negative respiratory pathogens and the host environment at the site of infection largely unknown. Pulmonary surfactant serves as an initial point of contact for inhaled bacteria entering the lung and is thought to contain molecular cues that aid colonization and pathogenesis. To gain insight into this ecological transition, we characterized the transcriptional responses of Pseudomonas aeruginosa PA14, Burkholderia thailandensis E264, Klebsiella pneumoniae MGH 78578, and Stenotrophomonas maltophilia K279A exposed to purified pulmonary surfactant (Survanta) through microarrays. This study provides novel insight into the interactions occurring between Gram-negative opportunistic pathogens and the host at an important infection site, and demonstrates the utility of purified lung surfactant preparations for dissecting host-lung pathogen interactions in vitro. The goal of this study was to compare the transcriptional responses of Pseudomonas aeruginosa PA14, Burkholderia thailandensis E264, Klebsiella pneumoniae MGH 78578, and Stenotrophomonas maltophilia K279A exposed to pulmonary surfactant using a custom affymetrix chip designed for their genomes. The goal of this study was to compare the transcriptional responses of Pseudomonas aeruginosa PA14, Burkholderia thailandensis E264, Klebsiella pneumoniae MGH 78578, and Stenotrophomonas maltophilia K279A exposed to pulmonary surfactant using a custom affymetrix chip designed for their genomes.
2018-03-30 | GSE110628 | GEO
Project description:We aim to compare global transcriptomic analysis of wt and delta-nrdRmutant in Pseudomonas aeruginosa PAO1 during aerobic and anaerobic conditions.
2016-06-27 | E-MTAB-3006 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa response to lung surfactant
| PRJNA212527 | ENA
Project description:b-Oxidative enzymes for fatty acid degradation (Fad) of long-chain fatty acid (LCFA), a component of lung surfactant phosphatidylcholine, are induced in vivo during lung infection in cystic fibrosis patients, which could contribute to nutrient acquisition and pathogenesis of Pseudomonas aeruginosa. In addition, fatty acid biosynthesis (Fab) is essential for the syntheses of two virulence controlling acylated-homoserine-lactone molecules in this organism. We mapped the promoter regions of the fadBA5-operon (PA3014 and PA3013) and a fadE homologue (PA2815) involved in Fad and the fabAB-operon involved in Fab. Focusing on the transposon mutagenesis of strain PAO1 carrying the PfadBA5-lacZ fusion, we identified a regulator for the fadBA5-operon to be PsrA (PA3006). Transcriptome analysis of the DpsrA mutant indicates its importance in regulating b-oxidative enzymes, which confirms a previous proteomic study. We further showed that induction of the fadBA-operon responds to LCFA signals, and this induction requires the presence of PsrA, suggesting that PsrA binds to LCFA to derepress fadBA5. Electrophoresis mobility shift assay indicate specific binding of PsrA to the fadBA5-promoter region. This binding is disrupted by specific LCFA (C18:1D9, C16:0, and to a lesser extent C14:0), but not by the first intermediate of b-oxidation, acyl-CoA. We proposed that PsrA is a Fad-regulator that binds and responds to LCFA signals in Pseudomonas aeruginosa. Keywords: Pseudomonas aeruginosa, wild-type PAO1 compared to PAO1-psrA::Tn
2008-02-14 | GSE8083 | GEO
Project description:b-Oxidative enzymes for fatty acid degradation (Fad) of long-chain fatty acid (LCFA), a component of lung surfactant phosphatidylcholine, are induced in vivo during lung infection in cystic fibrosis patients, which could contribute to nutrient acquisition and pathogenesis of Pseudomonas aeruginosa. In addition, fatty acid biosynthesis (Fab) is essential for the syntheses of two virulence controlling acylated-homoserine-lactone molecules in this organism. We mapped the promoter regions of the fadBA5-operon (PA3014 and PA3013) and a fadE homologue (PA2815) involved in Fad and the fabAB-operon involved in Fab. Focusing on the transposon mutagenesis of strain PAO1 carrying the PfadBA5-lacZ fusion, we identified a regulator for the fadBA5-operon to be PsrA (PA3006). Transcriptome analysis of the DpsrA mutant indicates its importance in regulating b-oxidative enzymes, which confirms a previous proteomic study. We further showed that induction of the fadBA-operon responds to LCFA signals, and this induction requires the presence of PsrA, suggesting that PsrA binds to LCFA to derepress fadBA5. Electrophoresis mobility shift assay indicate specific binding of PsrA to the fadBA5-promoter region. This binding is disrupted by specific LCFA (C18:1D9, C16:0, and to a lesser extent C14:0), but not by the first intermediate of b-oxidation, acyl-CoA. We proposed that PsrA is a Fad-regulator that binds and responds to LCFA signals in Pseudomonas aeruginosa. Experiment Overall Design: PAO1 and PAO1-psrA::Tn cultures grown in LB and cells were harvested at mid-log phase. Total RNA was isolated from both samples, and used for cDNA synthesis. And then, the cDNA for both samples were fragmented and labeled. The cDNA of PAO1 was used for 2 GeneChips, and PAO1-psrA::Tn cDNA was used for three GeneChips.
2008-04-07 | E-GEOD-8083 | biostudies-arrayexpress
Project description:One of the hallmarks of Pseudomonas aeruginosa cystic fibrosis (CF) infection is very high-cell-density (HCD) replication in the lung, allowing this bacterium to induce virulence controlled by HCD quorum-sensing systems. However, the nutrient sources sustaining HCD replication in this chronic infection is largely unknown. Hence, understanding the nutrient factors contributing to HCD in the CF lung will yield new insights into the 'metabolic pathogenicity' and potential treatment of CF infections caused by P. aeruginosa. Herein, we performed microarray studies of P. aeruginosa directly isolated from the CF lung to demonstrate its metabolic capability and virulence in vivo. Our in vivo microarray data, confirmed by real-time reverse-transcription-PCR, indicated P. aeruginosa expressed several genes for virulence, drug-resistance, and utilization of multiple nutrient sources (lung surfactant lipids and amino acids) contributing to HCD replication. The data also indicates deregulation of several pathways, suggesting in vivo evolution by deregulation of a large portion of the transcriptome during chronic CF infection. To our knowledge, this is the first in vivo transcriptome of P. aeruginosa in a natural CF infection, and it indicates several important aspects of pathogenesis, drug-resistance, and nutrient-utilization never before observed in vivo. Keywords: in vivo gene induction
2007-08-15 | GSE7704 | GEO
Project description:To determine if differences in the severity of pulmonary infection in cystic fibrosis been seen in late isolates od Pseudomonas aeruginosa and Burkholderia cepacia are associated with differences in the initial repsonse of alveolar macrophages (AM) to these pathogens, we assessed gene expression changes in human AM in response to infection with a laboratoty strain, early and late clinical isolates of P. aeruginosa, and B. cepacia. Experiment Overall Design: Alveolar macrophages were obtained from bronchoalveolar lavage. Experiment Overall Design: Two clinical strains isolated from the sputum of an individual with CF, AD2A and AD15B (provided by J. Burns, University of Washington, Seattle). AD2A is an early clinical isolate, and AD15B is a late clinical isolate; both were derived from the same individual.
2008-10-21 | E-GEOD-12245 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa is a major cause of morbidity and mortality in patients with cystic fibrosis (CF). The P. aeruginosa CF isolate PASS4 has reduced ability to catabolise various carbon sources however can grow on DNA as a sole carbon source but, with a higher biomass production than P. aeruginosa burns wound, laboratory strain PAO1. Therefore, proteomic profiling of PASS4 and PAO1 was conducted following growth on DNA as a sole carbon source. To compare the protein expression of P. aeruginosa strains PAO1 and PASS4 following growth in DNA, the amino acid, asparagine was used a control condition, as asparagine was one of the amino acids PASS4 could utilise.
2019-06-24 | PXD006742 | Pride
Project description:Cystic Fibrosis (CF) is the most common life limiting genetic disorder, characterized by chronic respiratory failure secondary to inflammation and chronic bacterial lung infection. Pseudomonas aeruginosa lung infection is associated with more severe lung disease and rapid progression of respiratory failure when compared to Staphylococcus aureus infection. We hypothesized that a specific signature of epigenetic factors targeting specific gene transcripts contributes to the increased morbidity seen in CF patients with chronic Pseudomonas infection. We collected exhaled breath condensate (EBC) from 27 subjects and evaluated miRNA signatures in these samples using commercial PCR array. We identified predicted mRNA targets and associated signaling pathways using Ingenuity Pathway Analysis. We found 11 differentially expressed miRNAs in EBC of patients infected with Pseudomonas aeruginosa compared to EBC from CF patients who were not chronically infected with Pseudomonas aeruginosa.
2019-04-22 | GSE130159 | GEO