Ontology highlight
ABSTRACT:
PROVIDER: PRJNA606771 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11235477_1.fastq.gz | Fastqsanger.gz |
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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.
2013-01-01 | GSE41926 | GEO
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:We use high-throughput sequencing to profile the response of the opportunistic fungal pathogen Candida albicans to mucins from the mucosal niche. We find that C. albicans undergoes a genome-wide phenotypic shift in response to mucins suppressing virulence-associated pathways.
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Project description:We use high-throughput sequencing to profile the response of the opportunistic fungal pathogen Candida albicans to mucins and mucin-glycans from the mucosal niche. We find that C. albicans undergoes a genome-wide phenotypic shift in response to mucins and their attached glycans suppressing virulence-associated pathways.
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Project description:S. epidermidis ability to form biofilms on indwelling medical devices and its association with the emergence of chronic infections is its main virulence factor. Nevertheless, it has been shown that the cells released from these biofilms are associated with the advent of serious acute infections with bacteraemia as one of the major clinical manifestations. Despite their clinical relevance, very little is known about the impact of biofilm-released cells in pathogenesis. Hence, herein, we characterized the murine immune response to the presence of cells released from S. epidermidis biofilms analysing spleen cells transcriptome by microarrays. These findings may help to explain the recurrent inflammatory symptoms presented by patients with colonization of indwelling medical devices.
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Project description:Staphylococcus epidermidis (SE) is one of the most common bacteria of the human skin microbiota. Despite its role as a commensal, SE has emerged as an opportunistic pathogen, associated with 80% of medical devices related infections. Moreover, these bacteria are extremely difficult to treat due to their ability to form biofilms and accumulate resistance to almost all classes of antimicrobials developed so far. Thus new preventive and therapeutic strategies are urgently needed. In spite of its clinical importance, the molecular mechanisms associated with SE colonisation and disease are still poorly understood. A deeper understanding of the metabolic and cellular processes associated with response to environmental factors characteristic of SE ecological niches in health and disease might provide new clues on colonisation and disease processes. Here we studied the impact of pH conditions, mimicking the skin pH (5.5) and blood pH (7.4), in a S. epidermidis commensal strain, belonging to the B clonal lineage, by means of next-generation proteomics and 1H NMR-based metabolomics. Moreover, we evaluated the metabolic changes occurring when a sudden pH change arise, simulating the skin barrier break produced by a catheter. We found that exposure of S. epidermidis to skin pH induced oxidative phosphorylation and biosynthesis of peptidoglycan, lipoteichoic acids and betaine. In contrast, at blood pH, the incorporation of monosaccharides and its oxidation by glycolysis and fermentation was promoted. Additionally, several proteins related to virulence and immune evasion, namely extracellular proteases and membrane iron transporters were more abundant at blood pH. In the situation of an abrupt skin-to-blood pH shift we observed the decrease in the osmolyte betaine and changes in the levels of several metabolites and proteins involved in redox cell homeostasis. Our results suggest that at the skin pH S. epidermidis cells are metabolically more active and adhesion is promoted, while at blood pH, metabolism is tuned down and cells have a more virulent profile. pH increase during commensal-to-pathogen conversion appears to be a critical environmental signal to the remodelling of the S. epidermidis metabolism towards a more pathogenic state. Targeting S. epidermidis proteins induced by a low alkaline pH and local acidification of medical devices microenvironment might be new strategies to treat and prevent S. epidermidis infections.
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