Ontology highlight
ABSTRACT:
PROVIDER: PRJNA704789 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13781800_1.fastq.gz | Fastqsanger.gz | |||
| SRR13781800_2.fastq.gz | Fastqsanger.gz | |||
| SRR13781801_1.fastq.gz | Fastqsanger.gz | |||
| SRR13781801_2.fastq.gz | Fastqsanger.gz | |||
| SRR13781802_1.fastq.gz | Fastqsanger.gz |
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Project description:Mycobacterium abscessus (Mab) causes serious infections that often require over 18 months of antibiotic combination therapy. With β lactam antibiotics being safe, double β-lactam and β-lactam/β-lactamase inhibitor combinations are of interest for improving treatment of Mab infections and minimizing toxicity. However, a mechanistic approach for building these combinations is lacking since little is known about which penicillin-binding protein (PBP) target receptors are inactivated by different β-lactams in Mab. This project aimed to identify PBPs in Mab and study the binding affinities of each of these PBPs with β-lactam antibiotics. These first PBP occupancy patterns in Mab provide a mechanistic foundation for selecting and optimizing safe and effective combination therapies with β-lactams.
2020-11-24 | PXD022644 | Pride
Project description:Pseudomonas aeruginosa is a predominant pathogen in chronic lung infections in individuals with cystic fibrosis (CF). Epidemic strains of P. aeruginosa, such as the Liverpool Epidemic Strain (LES), are capable of transferring between CF patients and have been associated with increased hospital visits and antibiotic treatments. We used label-free quantitative proteomics to compare the laboratory strain PAO1, beta-lactam resistant isolate LESB58, and beta-lactam susceptible isolate LESlike1 and their responses to three beta-lactams (aztreonam, carbenicillin, piperacillin), the aminoglycoside tobramycin, and hydrogen peroxide. Across all samples, we identified 3019 proteins with a minimum of two peptides. We found that LESB58 showed a large response to treatment with the beta-lactam carbenicillin, with 644 proteins significantly increased in abundance and 590 proteins significantly decreased in abundance (Students t-test, p≤0.05, FDR=0.05, S0=1). Proteomic characterization of an additional beta-lactam resistant isolate, LES431, exposed to carbenicillin showed that this response was shared by both isolates. Part of the response to carbenicillin in LESB58 included an increase in abundance in proteins involved in cell wall synthesis and division.
2023-08-23 | PXD034831 | Pride
Project description:Bactericidal antibiotics are powerful drugs because they not only inhibit essential bacterial functions, but convert them into toxic processes. Many bacteria are remarkably tolerant against antibiotics, due to inducible damage repair responses. How these responses promote whole population tolerance in important human pathogens is poorly understood. The two-component system VxrAB of the diarrheal pathogen Vibrio cholerae, a model system for tolerance against cell wall damaging (e.g., beta-lactam) antibiotics, is required for high-level beta-lactam tolerance. Here, we report the mechanism of VxrAB-mediated survival. We find that -lactam antibiotics inappropriately induce the Fur-regulated iron starvation response, causing an increase in intracellular free iron and colateral oxidative damage. VxrAB reduces antibiotic-induced toxic influx of Fe by downregulating iron importers and induces cell wall synthesis functions to counteract cell wall damage. Our results highlight the complex responses elicited by antibiotics and suggest that the ability to counteract diverse stresses promotes high-level antibiotic tolerance.
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Project description:Non-typeable Haemophilus influenzae (NTHi) is a common acute otitis media pathogen, with an incidence that is increased by previous antibiotic treatment. NTHi is also an emerging causative agent of other chronic infections in humans, some linked to morbidity, and all of which impose substantial treatment costs. In this study we explore the possibility that antibiotic exposure may stimulate biofilm formation by NTHi bacteria. We discovered that sub-inhibitory concentrations of beta-lactam antibiotic (i.e., amounts that partially inhibit bacterial growth) stimulated the biofilm-forming ability of NTHi strains, an effect that was strain and antibiotic dependent. When exposed to sub-inhibitory concentrations of beta-lactam antibiotics NTHi strains produced tightly packed biofilms with decreased numbers of culturable bacteria but increased biomass. The ratio of protein per unit weight of biofilm decreased as a result of antibiotic exposure. Antibiotic-stimulated biofilms had altered ultrastructure, and genes involved in glycogen production and transporter function were up regulated in response to antibiotic exposure. Down-regulated genes were linked to multiple metabolic processes but not those involved in stress response. Antibiotic-stimulated biofilm bacteria were more resistant to a lethal dose (10M-BM-5g/mL) of cefuroxime. Our results suggest that beta-lactam antibiotic exposure may act as a signaling molecule that promotes transformation into the biofilm phenotype. Loss of viable bacteria, increase in biofilm biomass and decreased protein production coupled with a concomitant up-regulation of genes involved with glycogen production might result in a biofilm of sessile, metabolically inactive bacteria sustained by stored glycogen. These biofilms may protect surviving bacteria from subsequent antibiotic challenges, and act as a reservoir of viable bacteria once antibiotic exposure has ended. 12 samples
2014-06-04 | E-GEOD-58213 | biostudies-arrayexpress
Project description:beta lactam resistance in Streptococcus pneumoniae
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Project description:Beta-lactam resistant isolates Genome sequencing
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Project description:Carbapenem-resistant Acinetobacter baumannii (CRAb) is an urgent public health threat, according to the CDC. This pathogen has few treatment options and causes severe nosocomial infections with >50% fatality rate. Although previous studies have examined the proteome of CRAb, there have been no focused analyses of dynamic changes to β-lactamase expression that may occur due to drug exposure. Here, we present our initial proteomic study of variation in β-lactamase expression that occurs in CRAb with different β-lactam antibiotics. Briefly, drug resistance to Ab (ATCC 19606) was induced by the administration of various classes of β-lactam antibiotics, and the cell-free supernatant was isolated, concentrated, separated by SDS-PAGE, digested with trypsin, and identified by label-free LC-MS-based quantitative proteomics. Thirteen proteins were identified and evaluated using a 1789 sequence database of Ab β-lactamases from UniProt, the majority of which were Class C β-lactamases (≥80%). Importantly, different antibiotics, even those of the same class (e.g. penicillin and amoxicillin), induced non-equivalent responses comprising various isoforms of Class C and D serine-β-lactamases, resulting in unique resistomes. These results open the door to a new approach of analyzing and studying the problem of multi-drug resistance in bacteria that rely strongly on β-lactamase expression.
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