Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1290306 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The study aimed to characterize plasmids mediating carbepenem resistance in Klebsiella pneumoniae in Pretoria, South Africa. We analysed 56 K. pneumoniae isolates collected from academic hospital around Pretoria. Based on phenotypic and molecular results of these isolates, 6 representative isolates were chosen for further analysis using long reads sequencing platform. We observed multidrug resistant phenotype in all these isolates, including resistance to aminoglycosides, tetracycline, phenicol, fosfomycin, floroquinolones, and beta-lactams antibiotics. The blaOXA-48/181 and blaNDM-1/7 were manily the plasmid-mediated carbapenemases responsible for carbapenem resistance in the K. pneumoniae isolates in these academic hospitals. These carbapenemase genes were mainly associated with plasmid replicon groups IncF, IncL/M, IncA/C, and IncX3. This study showed plasmid-mediated carbapenemase spread of blaOXA and blaNDM genes mediated by conjugative plasmids in Pretoria hospitals.
2019-10-17 | GSE138949 | GEO
Project description:The emergence of colistin resistance in carbapenem-resistant and extended-spectrum ß-lactamase (ESBL)-producing bacteria is a significant threat to human health, and new treatment strategies are urgently required. Here we investigated the ability of the safe-for-human use ionophore PBT2 to restore antibiotic sensitivity in several polymyxin-resistant, ESBL-producing, carbapenem resistant Gram-negative human pathogens. PBT2 was observed to resensitize Klebsiella pneumoniae, Escherichia coli, Acinetobacter baumannii, and Pseudomonas aeruginosa to last-resort polymyxin class antibiotics, including a ‘next generation’ polymyxin derivative, FADDI-287. To gain additional insight into the potential mechanism of action of PBT2, we analyzed the transcriptome of K. pneumoniae and E. coli in the presence of sub-inhibitory concentrations of PBT2. Treatment with PBT2 was associated with multiple stress responses in both K. pneumoniae and E. coli. Significant changes in the transcription of transition metal ion homeostasis genes were observed in both strains.
2019-06-13 | GSE132637 | GEO
Project description:The emergence and spread of polymyxin resistance, especially among Klebsiella pneumoniae isolates threaten the effective management of infections. This study profiled for polymyxin resistance mechanisms and investigated the activity of polymyxins plus vancomycin against carbapenem- and polymyxin-resistant K. pneumoniae.
2023-10-13 | PXD045685 | JPOST Repository
Project description:Klebsiella pneumoniae is an important human pathogen, causing various infections. Apart from traditional virulence factors, there remains a significant gap in the discovery and research of new chromosomal virulence factors. CpxR is a two-component system (TCS) response regulator, but its impact on the virulence of Klebsiella pneumoniae have not been conclusively determined. For the effect of CpxR on K. pneumoniae virulence, the cpxR deletion(ΔcpxR) strain exhibited reduced serum resistance and attenuated pathogenicity in both Galleria mellonella larvae and mouse infection models compared to the wild-type strain. To identify CpxR-regulated virulence genes, RNA-seq analysis was conducted, followed by deletion of transcription downregulated genes in the ΔcpxR strain. Through serum resistance assays and Galleria mellonella infection experiments, a novel potential virulence factor, KPHS_28080, was identified. Deletion of KPHS_28080 impaired serum survival and proliferation in carbapenem-resistant strains HS11286 and hypervirulent strain ATCC 43816. Furthermore, the ATCC 43816 ΔKPHS_28080 strain showed significantly reduced colonization, proliferation, and multi-organ dissemination capacity in mice, accompanied by diminished pathogenicity. The KPHS_28080 promoter contains a conserved CpxR binding motif, where CpxR binding enhances promoter activity and elevates gene transcription. Sequence alignment revealed that KPHS_28080 is widely conserved across Klebsiella pneumoniae strains, establishing it as a novel chromosome-encoded virulence factor. These results provide a new insight into the CpxR regulation of K. pneumoniae virulence and chromosomal virulence factors.
2025-07-10 | GSE300466 | GEO
Project description:Liao2011 - Genome-scale metabolic
reconstruction of Klebsiella pneumoniae (iYL1228)
This model is described in the article:
An experimentally validated
genome-scale metabolic reconstruction of Klebsiella pneumoniae
MGH 78578, iYL1228.
Liao YC, Huang TW, Chen FC,
Charusanti P, Hong JS, Chang HY, Tsai SF, Palsson BO, Hsiung
CA.
J. Bacteriol. 2011 Apr; 193(7):
1710-1717
Abstract:
Klebsiella pneumoniae is a Gram-negative bacterium of the
family Enterobacteriaceae that possesses diverse metabolic
capabilities: many strains are leading causes of
hospital-acquired infections that are often refractory to
multiple antibiotics, yet other strains are metabolically
engineered and used for production of commercially valuable
chemicals. To study its metabolism, we constructed a
genome-scale metabolic model (iYL1228) for strain MGH 78578,
experimentally determined its biomass composition,
experimentally determined its ability to grow on a broad range
of carbon, nitrogen, phosphorus and sulfur sources, and
assessed the ability of the model to accurately simulate growth
versus no growth on these substrates. The model contains 1,228
genes encoding 1,188 enzymes that catalyze 1,970 reactions and
accurately simulates growth on 84% of the substrates tested.
Furthermore, quantitative comparison of growth rates between
the model and experimental data for nine of the substrates also
showed good agreement. The genome-scale metabolic
reconstruction for K. pneumoniae presented here thus provides
an experimentally validated in silico platform for further
studies of this important industrial and biomedical
organism.
This model is hosted on
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and identified by:
MODEL1507180054.
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BioModels Database:
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To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-10-15 | BIOMD0000001094 | BioModels
Project description:Proteomic analysis of carbapenem-resistant Klebsiella pneumoniae exposure to tigecycline and aminoglycosides
2022-01-17 | PXD031030 |
Project description:Antibiotic use can lead to expansion of multi-drug resistant pathobionts within the gut microbiome that can cause life-threatening infections. Selective alternatives to conventional antibiotics are in dire need. Here, we describe a Klebsiella PhageBank that enables the rapid design of antimicrobial bacteriophage cocktails to treat multi-drug resistant Klebsiella pneumoniae. Using a transposon library in carbapenem-resistant K. pneumoniae, we identified host factors required for phage infection in major Klebsiella phage families. Leveraging the diversity of the PhageBank and experimental evolution strategies, we formulated combinations of phages that minimize the occurrence of phage resistance in vitro. Optimized bacteriophage cocktails selectively suppressed the burden of multi-drug resistant K. pneumoniae in the mouse gut microbiome and drove bacterial populations to lose key virulence factors that act as phage receptors. Further, phage-mediated diversification of bacterial populations in the gut enabled co-evolution of phage variants with higher virulence and a broader host range. Altogether, the Klebsiella PhageBank represents a roadmap for both phage researchers and clinicians to enable phage therapy against a critical multidrug-resistant human pathogen.
2024-10-01 | GSE272297 | GEO
Project description:Polymyxin B (PB) is introduced into the clinic as the last-line therapy against carbapenem-resistant <i>Klebsiella pneumoniae</i> (CRKP). Unfortunately, increased resistance to PB in <i>Klebsiella pneumoniae</i> (<i>K. pneumoniae</i>) has threatened global health. Resistance of <i>K. pneumoniae</i> to PB was induced by passaging in serial concentrations of PB and determined by microbroth dilution method. Growth characteristics of induced strains including growth curve, reversibility of resistance, and biofilm formation (crystal violet staining method) were measured. This study employed TMT-labeled quantitative proteomics and LC-MS/MS metabolomics analysis to investigate the key biological processes associated with PB resistance in <i>K. pneumoniae</i>. A total of 315 differentially expressed proteins (DEPs) were identified, of which 133 were upregulated and 182 were downregulated in the PB-resistant <i>K. pneumoniae</i>. KEGG enrichment analysis revealed that the DEPs were mainly involved in ATP-binding cassette (ABC) transporters and cationic antimicrobial peptide (CAMP) resistance. Proteins related to central carbon metabolism were inhibited in the PB-resistant <i>K. pneumoniae</i>, but proteins mediating LPS modification were activated. Transcriptional levels of CAMP resistance-related proteins were significantly different between PB-susceptible and -resistant <i>K. pneumoniae</i>. PB treatment led to an increase in reactive oxygen species (ROS) levels of <i>K. pneumoniae</i>. Metabolomics data demonstrated that 23 metabolites were significantly upregulated in PB-resistant <i>K. pneumoniae</i> and 5 were downregulated. The differential metabolites were mainly lipids, including glycerophospholipids, sphingolipids, and fatty acids. Exposure to PB resulted in increased level of phospholipid transport gene <i>mlaF</i> in <i>K. pneumoniae</i>. Our study suggested that membrane remodeling and inhibited central carbon metabolism are conducive to the development of PB resistance in <i>K. pneumoniae</i>.
2022-03-04 | MTBLS4132 | MetaboLights
Project description:This data set consists of pediatric acute lymphoblastic leukemia (ALL) primary bone marrow biopsies from the BC Children's Hospital BioBank, pediatric ALL cell lines, non-cancer bone marrow biopsies, and few ALL PDX. All files are DIA and searched by Spectronaut with a spectral library.
2023-01-05 | MSV000091012 | MassIVE