Group A Streptococcus antibiotic tolerance in necrotizing fasciitis
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB52606 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12917910_1.fastq.gz | Fastqsanger.gz | |||
| ERR12917910_2.fastq.gz | Fastqsanger.gz | |||
| ERR12917911_1.fastq.gz | Fastqsanger.gz | |||
| ERR12917911_2.fastq.gz | Fastqsanger.gz | |||
| ERR12917912_1.fastq.gz | Fastqsanger.gz |
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Project description:Streptococcal strains related to Necrotizing fasciitis
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Project description:Staphylococcus aureus is responsible for a substantial number of invasive infections globally each year. These infections are problematic because they are frequently recalcitrant to antibiotic treatment. Antibiotic tolerance, the ability of bacteria to persist despite normally lethal doses of antibiotics, contributes to antibiotic treatment failure in S. aureus infections. To understand how antibiotic tolerance is induced, S. aureus biofilms exposed to multiple anti-staphylococcal antibiotics were examined using both quantitative proteomics and transposon sequencing. These screens indicated that arginine metabolism is involved in antibiotic tolerance within a biofilm and led to the hypothesis that depletion of arginine within S. aureus communities can induce antibiotic tolerance. Consistent with this hypothesis, inactivation of argH, the final gene in the arginine synthesis pathway, induces antibiotic tolerance. Arginine restriction was found to induce antibiotic tolerance via inhibition of protein synthesis. In a mouse skin infection model, an argH mutant has enhanced ability to survive antibiotic treatment with vancomycin, highlighting the relationship between arginine metabolism and antibiotic tolerance during S. aureus infection. Uncovering this link between arginine metabolism and antibiotic tolerance has the potential to open new therapeutic avenues targeting previously recalcitrant S. aureus infections.
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Project description:Bacteria in biofilms have higher antibiotic tolerance than their planktonic counterparts. A major outstanding question is the degree to which the biofilm-specific cellular state and its constituent genetic determinants contribute to this hyper-tolerant phenotype. Here, using genome-wide functional profiling of a complex, heterogeneous mutant population of Pseudomonas aeruginosa MPAO1, we identified large sets of mutations that contribute to antibiotic tolerance predominantly in the biofilm or planktonic setting only. Our mixed population-based experimental design recapitulated the complexity of natural biofilms and, unlike previous studies, revealed clinically observed behaviors including the emergence of quorum sensing-deficient mutants. Our study revealed a substantial contribution of the cellular state to the antibiotic tolerance of biofilms, providing a rational foundation for the development of novel therapeutics against P. aeruginosa biofilm-associated infections. This dataset compares the expression of SAH108, a strain with enhanced antibiotic tolerance in the biofilm state, to expression in wild-type strains. We compared the expression of two biological replicates from strain SAH108 to samples from three wild-type, reference strains. All samples were collected from exponentially-growing planktonic cultures.
2011-11-21 | E-GEOD-26142 | biostudies-arrayexpress
Project description:Bacteria in biofilms have higher antibiotic tolerance than their planktonic counterparts. A major outstanding question is the degree to which the biofilm-specific cellular state and its constituent genetic determinants contribute to this hyper-tolerant phenotype. Here, using genome-wide functional profiling of a complex, heterogeneous mutant population of Pseudomonas aeruginosa MPAO1, we identified large sets of mutations that contribute to antibiotic tolerance predominantly in the biofilm or planktonic setting only. Our mixed population-based experimental design recapitulated the complexity of natural biofilms and, unlike previous studies, revealed clinically observed behaviors including the emergence of quorum sensing-deficient mutants. Our study revealed a substantial contribution of the cellular state to the antibiotic tolerance of biofilms, providing a rational foundation for the development of novel therapeutics against P. aeruginosa biofilm-associated infections. This dataset compares the expression of SAH108, a strain with enhanced antibiotic tolerance in the biofilm state, to expression in wild-type strains.
2011-11-21 | GSE26142 | GEO
Project description:Staphylococcus aureus is responsible for a substantial number of invasive infections globally each year. These infections are problematic because they are frequently recalcitrant to antibiotic treatment. Antibiotic tolerance, the ability of bacteria to persist despite normally lethal doses of antibiotics, contributes to antibiotic treatment failure in S. aureus infections. To understand how antibiotic tolerance is induced, S. aureus biofilms exposed to multiple anti-staphylococcal antibiotics were examined using both quantitative proteomics and transposon sequencing. These screens indicated that arginine metabolism is involved in antibiotic tolerance within a biofilm and led to the hypothesis that depletion of arginine within S. aureus communities can induce antibiotic tolerance. Consistent with this hypothesis, inactivation of argH, the final gene in the arginine synthesis pathway, induces antibiotic tolerance. Arginine restriction was found to induce antibiotic tolerance via inhibition of protein synthesis. In murine skin and bone infection models, an argH mutant has enhanced ability to survive antibiotic treatment with vancomycin, highlighting the relationship between arginine metabolism and antibiotic tolerance during S. aureus infection. Uncovering this link between arginine metabolism and antibiotic tolerance has the potential to open new therapeutic avenues targeting previously recalcitrant S. aureus infections.
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Project description:In order to explore the differentially expressed genes of E. coli B2 after citric acid induced antibiotic tolerance, we artificially induced the antibiotic tolerance of E. coli O157: H7 and verified its phenotype.
2023-02-26 | GSE225782 | GEO
Project description:In order to explore the differentially expressed genes of E. coli O157: H7 after citric acid induced antibiotic tolerance, we artificially induced the antibiotic tolerance of E. coli O157: H7 and verified its phenotype.
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Project description:Pseudomonas aeruginosa harbors sophisticated transcription factor (TF) networks to coordinately regulate cellular metabolic states for rapidly adapting to changing environments. The superior capacity in fine-tuning the metabolic states enables its success in tolerance to antibiotics and evading host immune defenses. However, the linkage among transcriptional regulation, metabolic states, and antibiotic tolerance in P. aeruginosa remains largely unclear. By screening the P. aeruginosa TF mutant library constructed by CRISPR/Cas12k-guided transposase, we identify that rccR (PA5438) is a major genetic determinant in aminoglycoside antibiotic tolerance, the deletion of which substantially enhances bacterial tolerance. We further reveal the inhibitory roles of RccR in pyruvate metabolism (aceE/F) and glyoxylate shunt pathway (aceA and glcB), and overexpression of aceA or glcB enhances bacterial tolerance. Moreover, we identify that 2-keto-3-deoxy-6-phosphogluconate (KDPG) is a signal molecule that directly binds to RccR. Structural analysis of the RccR/KDPG complex reveals the detailed interactions. Substitution of the key residues R152, K270, or R277 with alanine abolishes KDPG sensing by RccR and impairs bacterial growth with glycerol or glucose as the sole carbon source. Collectively, our study unveils the connection between aminoglycoside antibiotic tolerance and RccR-mediated central carbon metabolism regulation in P. aeruginosa, and elucidates the KDPG sensing mechanism by RccR.
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Project description:Antibiotics are a triumph of modern medicine, but their power to cure infections is being eroded through the evolution and dissemination of resistance. Evolution of genetic resistance is in part facilitated by non-genetic resistance mechanisms that increase antibiotic tolerance buying time for evolutionary innovation. Using live cell imaging, we discovered that Escherichia coli treated with aminoglycosides permanently lose the ability to divide within 4 hours, yet a majority of cells maintain membrane integrity and metabolic 2 days post treatment, and some continuing activity for up to > 4 days post treatment – a bacterial senescent-like state. These cells, which we term zombies, exhibit dynamic gene expression and metabolomic profiles even after exiting the cell cycle. Gene expression data revealed upregulated the phage shock protein response maintained membrane integrity. Remarkably, these zombie cells, though unable to form new colonies, increase antibiotic tolerance of treatment-naïve cells, implying chemical communication. Chemical supplementation and genetic knockouts showed that zombies communicate to treatment-naïve cells by secreting indole. In summary, our study revealed a bacterial senescent-like state, induced by aminoglycosides, that modifies the antibiotic tolerance of multiple bacterial species.
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