Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1242271 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32865946_1.fastq.gz | Fastqsanger.gz | |||
| SRR32865946_2.fastq.gz | Fastqsanger.gz | |||
| SRR32865947_1.fastq.gz | Fastqsanger.gz | |||
| SRR32865947_2.fastq.gz | Fastqsanger.gz | |||
| SRR32865948_1.fastq.gz | Fastqsanger.gz |
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Project description:Antimicrobial Resistance and the Environment - Sources, Persistence, Transmission and Risk Management.
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Project description:Antimicrobial Resistance and the Environment - Sources, Persistence, Transmission and Risk Management.
| PRJEB47048 | ENA
Project description:Bacterial evolution of antibiotic resistance frequently has deleterious side effects on microbial growth, virulence, and susceptibility to other antimicrobial agents. However, it is unclear how these trade-offs could be utilized for manipulating antibiotic resistance in the clinic, not least because the underlying molecular mechanisms are poorly understood. Using laboratory evolution, we demonstrate that clinically relevant resistance mutations in Escherichia coli constitutively rewire a large fraction of the transcriptome in a repeatable and stereotypic manner. Strikingly, lineages adapted to functionally distinct antibiotics and having no resistance mutations in common show a wide range of parallel gene expression changes that alter oxidative stress response, iron homeostasis, and the composition of the bacterial outer membrane and cell surface. These common physiological alterations are associated with changes in cell morphology and enhanced sensitivity to antimicrobial peptides. Finally, the constitutive transcriptomic changes induced by resistance mutations are largely distinct from those induced by antibiotic stresses in the wild-type. This indicates a limited role for genetic assimilation of the induced antibiotic stress response during resistance evolution. Our work suggests that diverse resistance mutations converge on similar global transcriptomic states that shape genetic susceptibility to antimicrobial compounds.
2023-01-26 | GSE223493 | GEO
Project description:CroRS is a cell envelope stress response two-component system in the bacterial pathogen Enterococcus faecalis. Antimicrobial tolerance is the ability of an organism to survive, but not proliferate, upon antimicrobial challenge, and is a known precursor to the development of antimicrobial resistance. We have previously shown that CroRS is essential for antimicrobial tolerance in E. faecalis. Therefore, the aim of this experiment was to determine the teixobactin-induced CroRS regulon to identify key pathways of antimicrobial tolerance. To do this, E. faecalis wild-type and a croRS deletion mutant were grown to mid-exponential phase and challenged with and without teixobactin (0.5 ug/ml) for 1 hour. RNA was subsequently extracted, purified and RNA sequenced. RNA libraries were prepped using the Zymo-Seq RiboFree Total RNA-Seq Library Kit. Sequencing was completed using an Illumina MiSeq (v3) system generating 150 bp paired-end reads.
2023-09-22 | E-MTAB-12526 | biostudies-arrayexpress
Project description:We have shown that, in acute models of vaccination, the antimicrobial peptide cathelicidin potentiates Th17 cell differentiation. TO examine this in long-term, chronic inflammation, here we studied T cells in the mouse model of Multiple Sclerosis. We examined T cells from wildtype mice and those lacking cathelicidin.
2021-11-14 | GSE188655 | GEO
Project description:Pseudomonas aeruginosa colonises the upper airway of cystic fibrosis (CF) patients, providing a reservoir of host-adapted genotypes that subsequently establish chronic lung infection. We previously experimentally-evolved P. aeruginosa in a murine model of respiratory tract infection and observed mutations in pmrB that promoted establishment and persistence of infection. Here we show that mutations in pmrB, which encodes the sensor kinase of the PmrAB two-component system, are acquired early in infection and increase resistance to the host antimicrobial lysozyme. Proteomic analysis of pmrB mutants reveal downregulation of proteins involved in LPS biosynthesis, antimicrobial resistance and phenazine production, and upregulation of proteins involved in adherence, lysozyme resistance and inhibition of the chloride ion channel CFTR, relative to wild-type strain LESB65. Accordingly, pmrB mutants show enhanced adherence to airway epithelial cells and downregulate host CFTR expression. P. aeruginosa pmrB mutations are found in CF patient isolates and are associated with the same phenotypes, but are subject to an evolutionary trade-off: enhanced colonisation potential, resistance to host defences and CFTR inhibition, but concomitant increased susceptibility to antibiotics.
2018-07-11 | PXD009705 | Pride
Project description:<p>The study of antimicrobial resistance (AMR) in infectious diarrhea has generally been limited to cultivation, antimicrobial susceptibility testing and targeted PCR assays. When individual strains of significance are identified, whole genome shotgun (WGS) sequencing of important clones and clades is performed. Genes that encode resistance to antibiotics have been detected in environmental, insect, human and animal metagenomes and are known as "resistomes". While metagenomic datasets have been mined to characterize the healthy human gut resistome in the Human Microbiome Project and MetaHIT and in a Yanomani Amerindian cohort, directed metagenomic sequencing has not been used to examine the epidemiology of AMR. Especially in developing countries where sanitation is poor, diarrhea and enteric pathogens likely serve to disseminate antibiotic resistance elements of clinical significance. Unregulated use of antibiotics further exacerbates the problem by selection for acquisition of resistance. This is exemplified by recent reports of multiple antibiotic resistance in Shigella strains in India, in Escherichia coli in India and Pakistan, and in nontyphoidal Salmonella (NTS) in South-East Asia. We propose to use deep metagenomic sequencing and genome level assembly to study the epidemiology of AMR in stools of children suffering from diarrhea. Here the epidemiology component will be surveillance and analysis of the microbial composition (to the bacterial species/strain level where possible) and its constituent antimicrobial resistance genetic elements (such as plasmids, integrons, transposons and other mobile genetic elements, or MGEs) in samples from a cohort where diarrhea is prevalent and antibiotic exposure is endemic. The goal will be to assess whether consortia of specific mobile antimicrobial resistance elements associate with species/strains and whether their presence is enhanced or amplified in diarrheal microbiomes and in the presence of antibiotic exposure. This work could potentially identify clonal complexes of organisms and MGEs with enhanced resistance and the potential to transfer this resistance to other enteric pathogens.</p> <p>We have performed WGS, metagenomic assembly and gene/protein mapping to examine and characterize the types of AMR genes and transfer elements (transposons, integrons, bacteriophage, plasmids) and their distribution in bacterial species and strains assembled from DNA isolated from diarrheal and non-diarrheal stools. The samples were acquired from a cohort of pediatric patients and controls from Colombia, South America where antibiotic use is prevalent. As a control, the distribution and abundance of AMR genes can be compared to published studies where resistome gene lists from healthy cohort sequences were compiled. Our approach is more epidemiologic in nature, as we plan to identify and catalogue antimicrobial elements on MGEs capable of spread through a local population and further we will, where possible, link mobile antimicrobial resistance elements with specific strains within the population.</p>
| phs001260 | dbGaP
Project description:Enterococcus faecalis is a Gram-positive bacterium that is a major cause of hospital-acquired infections due to its intrinsic resistance to cell wall-active antimicrobials. One critical determinant of this resistance is the transmembrane kinase IreK, which belongs to the PASTA kinase family of bacterial signaling proteins involved with the regulation of cell wall homeostasis. IreK has enhanced activity in response to cell wall stress, but direct substrates of IreK phosphorylation leading to antimicrobial resistance are largely unknown. To better understand stress-modulated phosphorylation events contributing to virulence, wild type E. faecalis treated with cell wall-active chlorhexidine and ceftriaxone were examined via phosphoproteomics. Among the most prominent changes were increased phosphorylation of divisome components after both treatments, implicating cell division proteins in antimicrobial defense signaling. Phosphorylation mediated by IreK was then determined via similar analysis with a E. faecalis ΔireK mutant strain, revealing potential IreK substrates involved with the formation/maintenance of biofilms and within the E. faecalis two-component system, another common signal transduction pathway for antimicrobial resistance. These results reveal critical insights into the biological functions of IreK and the mechanisms of E. faecalis antimicrobial resistance.
2021-11-03 | PXD023265 | Pride