Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1012888 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25905707.fastq.gz | Fastqsanger.gz | |||
| SRR25905708.fastq.gz | Fastqsanger.gz | |||
| SRR25905709.fastq.gz | Fastqsanger.gz | |||
| SRR25905710.fastq.gz | Fastqsanger.gz | |||
| SRR25905711.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Elexacaftor/tezacaftor/ivacaftor (ETI, Trikafta) is highly effective treatment for many cystic fibrosis patients, at least partly because it increases CFTR mediated Cl- and HCO3- secretion by airway epithelial cells leading to improved lung function and less frequent exacerbations and hospitalizations. However, little is known about how ETI affects airway epithelial cells in ways not related to CFTR mediated Cl- and HCO3- secretion, for example how ETI affects the expression of genes other than CFTR or how ETI might affect airway cells’ response to infection. It is established that CF airway cells bearing the delta F 508 mutation the CFTR gene respond characteristically differently from wild type CFTR cells, and we hypothesized that, as a highly effective CFTR modulator, ETI might make airway cells from CF donors respond to pathogen stimulation (Pseudomonas aeruginosa PA14 or outer membrane vesicles isolated from these bacteria) in more the same way that cells from wild type, healthy control cells do. We tested this hypothesis by measuring gene expression responses in polarized primary CF airway cells exposed to ETI alone or ETI in the presence of a pathogen challenge (PA14 or outer membrane vesicles). Responses of CFTR wild type primary CF airway cells to PA14 or outer membrane vesicles was also measured for comparison
2024-06-25 | GSE268718 | GEO
Project description:The surge of antimicrobial resistance in recent decades threatens efficacy of current antibiotics, particularly against Pseudomonas aeruginosa, a highly resistant gram-negative pathogen. The asymmetric outer membrane of P. aeruginosa combined with its array of efflux pumps provide a barrier to xenobiotic intracellular accumulation, thus making the discovery of novel drugs with whole cell antibacterial activity very challenging. We adapted PROSPECT, a genome-wide, target-based, whole cell screening strategy, to take a focused approach to discover small molecule probes with specific activity against engineered P. aeruginosa mutants depleted for essential proteins localized at the outer membrane. We identified BRD1401, a small molecule that has specific activity against a P. aeruginosa mutant depleted for the essential lipoprotein, OprL. Genetic studies identified a novel link between OprL and the non-essential, outer membrane β barrel protein, OprH, to modulate BRD1401 activity. BRD1401 directly bound to OprH to disrupt the known interaction between OprH and lipopolysaccharide (LPS) in vitro and in whole bacteria. OprH also biochemically interacted with OprL, thus providing a link between outer membrane and peptidoglycan in P. aeruginosa. Thus, a whole cell, multiplexed screen against P. aeruginosa identified a species-specific inhibitor and probe molecule that revealed novel pathogen biology.
2024-03-15 | GSE252756 | GEO
Project description:The surge of antimicrobial resistance in recent decades threatens efficacy of current antibiotics, particularly against Pseudomonas aeruginosa, a highly resistant gram-negative pathogen. The asymmetric outer membrane of P. aeruginosa combined with its array of efflux pumps provide a barrier to xenobiotic intracellular accumulation, thus making the discovery of novel drugs with whole cell antibacterial activity very challenging. We adapted PROSPECT, a genome-wide, target-based, whole cell screening strategy, to take a focused approach to discover small molecule probes with specific activity against engineered P. aeruginosa mutants depleted for essential proteins localized at the outer membrane. We identified BRD1401, a small molecule that has specific activity against a P. aeruginosa mutant depleted for the essential lipoprotein, OprL. Genetic studies identified a novel link between OprL and the non-essential, outer membrane β barrel protein, OprH, to modulate BRD1401 activity. BRD1401 directly bound to OprH to disrupt the known interaction between OprH and lipopolysaccharide (LPS) in vitro and in whole bacteria. OprH also biochemically interacted with OprL, thus providing a link between outer membrane and peptidoglycan in P. aeruginosa. Thus, a whole cell, multiplexed screen against P. aeruginosa identified a species-specific inhibitor and probe molecule that revealed novel pathogen biology.
2024-03-15 | GSE254108 | GEO
Project description:Cell-surface signaling is a sophisticated regulatory mechanism used by gram-negative bacteria to sense signals from outside the cell and transmit them into the cytoplasm. This regulatory system consists of an outer membrane-localized TonB-dependent receptor (TonB-dependent transducer), a cytoplasmic membrane-localized anti-sigma factor and an extracytoplasmic function (ECF) sigma factor. By microarray analysis we have identified the regulons of four novel P. aeruginosa signaling systems. For that, the ECF sigmas PA0149, PA2050, PA2093 and PA4896 have been overexpressed in P. aeruginosa and their target gene candidates have been identified using DNA microarray. Keywords: Overexpression of ECF sigma factors
2007-11-24 | GSE9657 | GEO
Project description:Cell-surface signaling is a sophisticated regulatory mechanism used by gram-negative bacteria to sense signals from outside the cell and transmit them into the cytoplasm. This regulatory system consists of an outer membrane-localized TonB-dependent receptor (TonB-dependent transducer), a cytoplasmic membrane-localized anti-sigma factor and an extracytoplasmic function (ECF) sigma factor. By microarray analysis we have identified the regulons of four novel P. aeruginosa signaling systems. For that, the ECF sigmas PA0149, PA2050, PA2093 and PA4896 have been overexpressed in P. aeruginosa and their target gene candidates have been identified using DNA microarray. Experiment Overall Design: Five different samples are analyzed namely P. aeruginosa (pMMB67EH) (control/reference sample), P. aeruginosa (pMMB-PA4896) (overexpressing the PA4896 ECF sigma factor), P. aeruginosa (pMMB-PA0149) (overexpressing the PA0149 ECF sigma factor), P. aeruginosa (pMMB-PA2050) (overexpressing the PA2050 ECF sigma factor), and P. aeruginosa (pMMB-PA2093) (overexpressing the PA2093 ECF sigma factor). Two different replicates are included for the three first samples and one for the two last samples.
2008-06-16 | E-GEOD-9657 | biostudies-arrayexpress
Project description:Escherichia coli Outer Membrane Vesicles RNA studies
| PRJNA234345 | ENA
Project description:short RNA-Seq of Pseudomonas aeruginosa outer membrane vesicles (OMVs) and whole cells
| PRJNA291596 | ENA
Project description:Kaiser2014 - Salmonella persistence after ciprofloxacin treatment
The model describes the bacterial tolerance to antibiotics. Using a mouse model for Salmonella diarrhea, the authors have found that bacterial persistence occurs in the presence of the antibiotic ciprofloxacin because Salmonella can exist in two different states. One, the fast-growing population that spreads in the host's tissues and the other, slow-growing "persister" population that hide out inside dendritic cells of the host's immune system and cannot be attacked by the antibiotics. However, this can be killed by adding agents that directly stimulate the host's immune defense.
This model is described in the article:
Cecum lymph node dendritic cells harbor slow-growing bacteria phenotypically tolerant to antibiotic treatment.
Kaiser P, Regoes RR, Dolowschiak T, Wotzka SY, Lengefeld J, Slack E, Grant AJ, Ackermann M, Hardt WD.
PLoS Biol. 2014 Feb 18;12(2):e1001793.
Abstract:
In vivo, antibiotics are often much less efficient than ex vivo and relapses can occur. The reasons for poor in vivo activity are still not completely understood. We have studied the fluoroquinolone antibiotic ciprofloxacin in an animal model for complicated Salmonellosis. High-dose ciprofloxacin treatment efficiently reduced pathogen loads in feces and most organs. However, the cecum draining lymph node (cLN), the gut tissue, and the spleen retained surviving bacteria. In cLN, approximately 10%-20% of the bacteria remained viable. These phenotypically tolerant bacteria lodged mostly within CD103⁺CX₃CR1⁻CD11c⁺ dendritic cells, remained genetically susceptible to ciprofloxacin, were sufficient to reinitiate infection after the end of the therapy, and displayed an extremely slow growth rate, as shown by mathematical analysis of infections with mixed inocula and segregative plasmid experiments. The slow growth was sufficient to explain recalcitrance to antibiotics treatment. Therefore, slow-growing antibiotic-tolerant bacteria lodged within dendritic cells can explain poor in vivo antibiotic activity and relapse. Administration of LPS or CpG, known elicitors of innate immune defense, reduced the loads of tolerant bacteria. Thus, manipulating innate immunity may augment the in vivo activity of antibiotics.
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2024-09-02 | BIOMD0000000527 | BioModels