Pseudomonas aeruginosa
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ABSTRACT:
PROVIDER: PRJNA109057 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the following subset Series:; GSE9989: Tobramycin Treatment of P. aeruginosa Biofilms Grown on CFBE41o- Cells; GSE9991: Tobramycin Treatment of Planktonic Pseudomonas aeruginosa Experiment Overall Design: Refer to individual Series
2008-06-18 | E-GEOD-10030 | biostudies-arrayexpress
Project description:We grew Pseudomonas aeruginosa biofilms on CFBE41o- human airway cells in culture, and we treated these biofilms with tobramycin. Microarray analysis was performed to gain an understanding of the global transcriptional changes that occur during antibiotic treatment. Experiment Overall Design: We compared three untreated control samples with three tobramycin-treated samples. Biofilms were grown on CFBE41o- cells in culture for 9 hours in MEM/0.4% arginine. Replicate samples were then incubated in the presence or absence of 500 μg/mL tobramycin for 30 minutes.
2008-06-18 | E-GEOD-9989 | biostudies-arrayexpress
Project description:We grew Pseudomonas aeruginosa biofilms on CFBE41o- human airway cells in culture, and we treated these biofilms with tobramycin. Microarray analysis was performed to gain an understanding of the global transcriptional changes that occur during antibiotic treatment. Keywords: Antibiotic Response
2008-06-10 | GSE9989 | GEO
Project description:As a comparison to tobramycin-treated P. aeruginosa biofilms, we investigated the response of planktonic P. aeruginosa to tobramycin by microarray. Keywords: Tobramycin Response
2008-06-10 | GSE9991 | GEO
Project description:In the clinical setting, mutations in the CFTR gene enhance the inflammatory response to P. aeruginosa (PA01) infection, but measurements of the inflammatory response to pathogen stimulation by isolated airway epithelia can yield variable results. In this series, we exposed CFBE41o- cells over-expressing ∆F508/∆F508 CFTR and CFBE41o- cells rescued with wt-CFTR to P. aeruginosa biofilms. P. aeruginosa elicited a more robust increase in cytokine and chemokine expression (e.g., IL-8, CXCL2, CXCL3, CXCR4 and TNF-α) in CFBE-wt-CFTR cells compared to CFBE-∆F508-CFTR cells. These results demonstrate that CFBE41o- cells complemented with wt-CFTR mount a more robust inflammatory response to P. aeruginosa than CFBE41o- ∆F508/∆F508-CFTR cells.
2011-08-01 | GSE30439 | GEO
Project description:The aim of this study is to evaluate the evolutionary robustness of the quorum sensing inhibitor (QSI) furanone C-30 for the treatment of P. aeruginosa biofilm infections. We repeatedly exposed P. aeruginosa biofilms to furanone C-30 (with or without tobramycin) in the synthetic cystic fibrosis sputum medium (SCFM2) and characterized the genotype and phenotype of the evolved lineages. P. aeruginosa biofilms were grown in SCFM2 for 24 h after which the treatment in fresh SCFM2 was added to obtain a final concentration of 20 µg/ml tobramycin and 100 µg/ml furanone C-30. The negative control was treated with fresh SCFM2, including the same amount of DMSO (0.25%) as for the biofilms treated with C-30. After 24 h of static incubation at 37°C, biofilms were sonicated and vortexed in order to disintegrate the biofilm aggregates. After each cycle the number of CFU was determined and an aliquot of the culture was stored at -80°C in Microbank vials to allow further tests on the evolved strains. A sample from the treated biofilm was used to prepare a new overnight culture, in order to start a new cycle. For each treatment three independent lineages were established, that were each exposed for 16 cycles. Whole-genome sequencing was performed on the wild type P. aeruginosa PAO1 and on the exposed lineages after 5, 10 and 16 cycles.
2021-03-05 | E-MTAB-10124 | biostudies-arrayexpress
Project description:As a comparison to tobramycin-treated P. aeruginosa biofilms, we investigated the response of planktonic P. aeruginosa to tobramycin by microarray. Experiment Overall Design: We included 2 control (untreated) cultures and 2 tobramycin-treated cultures. We used mid-exponential phase cultures of P. aeruginosa PA14. Replicate cultures were incubated in the presence or absence of 5 μg/mL tobramycin for 30 minutes at 37°C.
2008-06-21 | E-GEOD-9991 | biostudies-arrayexpress
Project description:Chronic infections with Pseudomonas aeruginosa are a leading cause of morbidity and mortality in persons with cystic fibrosis (pwCF). P. aeruginosa persists in the CF lung by utilizing adaptation strategies to cause infection, including altering the expression of metabolic genes to acquire nutrients that are abundant in the CF airway. Glycerol in the airway is imported and metabolized by the glp regulon, which is under the control of the GlpR repressor. It has been shown that the loss of GlpR results in increased biofilm development in P. aeruginosa CF isolate compared to a wound isolate. Based on the increased biofilm phenotype observed and because biofilms are associated with increased antibiotic tolerance, we questioned whether GlpR plays a role in mediating antibiotic resistance of P. aeruginosa. We measured tobramycin tolerance in wild-type and glpR-defective P. aeruginosa isolates from the CF airway (FRD1) and a wound (PAO1). Cultures were grown in lysogeny broth or synthetic cystic fibrosis sputum consisting of the base formula of primarily amino acids (SCFM1) or supplemented with mucins and DNA (SCFM2), with dose-dependent concentrations of tobramycin. We tested the impact of a glpR mutation on P. aeruginosa adherence on bronchial epithelial cells from pwCF (CFBE) in the presence of tobramycin. CFBE cells were inoculated at an MOI of ~1:20 for 1 hour, given fresh apical media for 5 more hours, then apical and basal media was replaced with media containing 20 µg/ml tobramycin. We measured colony forming units (CFUs) and lactate dehydrogenase (LDH) release for cytotoxicity. Loss of glpR increased tolerance to tobramycin in both the PAO1 and FRD1 backgrounds in vitro at a concentration of 0.625 µg/mL in lysogeny broth and SCFM1. On both CFBE’s and 16HBE’s, the antibiotic resistance phenotype was more prominent in FRD1 glpR with a 2-log increase in viable bacteria when grown on cells and treated with 20 ug/ml tobramycin. However, changes in cytotoxicity where not observed between wildtype and GlpR mutants as LDH measurements were not significantly different. Our results indicate that GlpR may regulate antibiotic tolerance, in addition to biofilm development and glycerol metabolism. Additional studies are necessary to determine the mechanism of how GlpR modulates biofilm development and antibiotic tolerance.
2025-09-05 | GSE280261 | GEO
Project description:In the clinical setting, mutations in the CFTR gene enhance the inflammatory response to P. aeruginosa (PA01) infection, but measurements of the inflammatory response to pathogen stimulation by isolated airway epithelia can yield variable results. In this series, we exposed CFBE41o- cells over-expressing ?F508/?F508 CFTR and CFBE41o- cells rescued with wt-CFTR to P. aeruginosa biofilms. P. aeruginosa elicited a more robust increase in cytokine and chemokine expression (e.g., IL-8, CXCL2, CXCL3, CXCR4 and TNF-?) in CFBE-wt-CFTR cells compared to CFBE-?F508-CFTR cells. These results demonstrate that CFBE41o- cells complemented with wt-CFTR mount a more robust inflammatory response to P. aeruginosa than CFBE41o- ?F508/?F508-CFTR cells. CFBE41o- cells generously provided by Dr. J.P. Clancy (University of Alabama). The series involved 4 treatment groups: unexposed wild type CFTR cells, unexposed ?F508/?F508 CFTR cells, wild type CFTR cells exposed to PA01, and ?F508/?F508 CFTR cells exposed to PA01. Each treatment group involved 4 replicate polarized monolayers. PAO1 was added to the apical side of exposed monolayers at a multiplicity of infection (MOI) of 30:1 for 1 hour in the absence of antibiotics, and then planktonic PAO1 was removed by replacing the apical medium with MEM supplemented with 0.4% arginine (2). Control monolayers were treated identically except that vehicle only (medium used to grow PAO1, MEM supplemented with 0.4% arginine) was added to the apical side of cells. Five hours after washing planktonic P. aeruginosa from the cell monolayers mRNA was isolated.
2011-07-31 | E-GEOD-30439 | biostudies-arrayexpress
Project description:Bacteria growing in biofilms are physiologically heterogeneous, due in part to their adaptation to local environmental conditions. Here, we characterized the local transcriptional responses of Pseudomonas aeruginosa growing in biofilms by using microarray analysis of isolated biofilm subpopulations. The results demonstrated that cells at the top of the biofilms had high mRNA abundances for genes involved in general metabolic functions, while mRNAs for these housekeeping genes were low in cells at the bottom of the biofilms. Selective GFP labeling showed that cells at the top of the biofilm were actively dividing. However, the dividing cells had high mRNAs levels for genes regulated by the hypoxia induced regulator, Anr. Slow-growing cells deep in the biofilms had little expression of Anr-regulated genes and may have experienced long-termanoxia. Transcripts for ribosomal proteins were primarily associated with the metabolically active cell fraction, while ribosomal RNAs were abundant throughout the biofilms, indicating that ribosomes are stably maintained even in slowly growing cells. Consistent with these results was the identification of mRNAs for ribosome hibernation factors (rmf and PA4463) at the bottom of the biofilms. A P. aeruginosa ∆rmf strain had increased uptake of the membrane integrity stain, propidium iodide. Using selective GFP labeling and cell sorting, we showed that the dividing cells were more susceptible to tobramycin and ciprofloxacin than the dormant subpopulation. The results demonstrate that in thick P. aeruginosa biofilms, cells are physiologically distinct spatially, with cells deep in the biofilm in a viable but antibiotic-tolerant slow-growth state.
2012-05-03 | GSE34762 | GEO