Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1235639 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Aminoglycoside resistance in Escherichia coli
| PRJNA607301 | ENA
Project description:Human Peptidoglycan Recognition Proteins (PGRPs) kill bacteria, likely by over-activating stress responses in bacteria. To gain insight into the mechanism of PGRP killing of Escherichia coli and bacterial defense against PGRP killing, gene expression in E. coli treated with a control protein (bovine serum albumin, BSA), human recombinant PGRP (PGLYRP4), gentamicin (aminoglycoside antibiotic), and CCCP (membrane potential decoupler) were compared. Each treatment induced unique and somewhat overlapping pattern of gene expression. PGRP highly increased expression of genes for oxidative and disulfide stress, detoxification and efflux of Cu, As, and Zn, repair of damaged proteins and DNA, methionine and histidine synthesis, energy generation, and Fe-S clusters repair. PGRP also caused marked decrease in the expression of genes for Fe uptake and motility. Gene expression microarray in E. coli exposed to a human bactericidal innate immunity protein, PGRP, showed induction of oxidative stress response and defense genes, with different expression pattern than E. coli exposed to an aminoglycoside antibiotic and a membrane potential decoupler.
2014-07-25 | GSE44211 | GEO
Project description:The gene encoding elongation factor G, fusA1, is frequently mutated in clinical isolates of Pseudomonas aeruginosa from patients with cystic fibrosis. Recent work has shown that fusA1 mutants often display elevated aminoglycoside resistance due to increased expression of the aminoglycoside efflux pump, MexXY. We isolated a spontaneous gentamicin-resistant fusA1 mutant (FusA1-P443L) in which mexXY expression was increased. We compared the transcriptome of this fusA1 mutant (EMC1) with the P. aeruginosa PAO1-derived progenitor strain (EMC0) and complemented mutant strain expressing the wild-type fusA1 gene in trans (EMC1*).
2020-09-16 | E-MTAB-8690 | biostudies-arrayexpress
Project description:Human Peptidoglycan Recognition Proteins (PGRPs) kill bacteria, likely by over-activating stress responses in bacteria. To gain insight into the mechanism of PGRP killing of Escherichia coli and bacterial defense against PGRP killing, gene expression in E. coli treated with a control protein (bovine serum albumin, BSA), human recombinant PGRP (PGLYRP4), gentamicin (aminoglycoside antibiotic), and CCCP (membrane potential decoupler) were compared. Each treatment induced unique and somewhat overlapping pattern of gene expression. PGRP highly increased expression of genes for oxidative and disulfide stress, detoxification and efflux of Cu, As, and Zn, repair of damaged proteins and DNA, methionine and histidine synthesis, energy generation, and Fe-S clusters repair. PGRP also caused marked decrease in the expression of genes for Fe uptake and motility. Gene expression microarray in E. coli exposed to a human bactericidal innate immunity protein, PGRP, showed induction of oxidative stress response and defense genes, with different expression pattern than E. coli exposed to an aminoglycoside antibiotic and a membrane potential decoupler. E. coli was treated with PGRP (human recombinant PGLYRP4), gentamicin, or CCCP (carbonyl cyanide 3-chlorophenylhydrazone). RNA was obtained from each culture and assayed for gene expression using whole genome Affymetrix E. coli Genome 2.0 Array. Each experiment was repeated 3 times.
2014-07-25 | E-GEOD-44211 | biostudies-arrayexpress
Project description:The gene encoding elongation factor G, fusA1, is frequently mutated in clinical isolates of Pseudomonas aeruginosa from patients with cystic fibrosis. Recent work has shown that fusA1 mutants often display elevated aminoglycoside resistance due to increased expression of the aminoglycoside efflux pump, MexXY. We isolated a spontaneous gentamicin-resistant fusA1 mutant (FusA1-P443L) in which mexXY expression was increased. We compared the proteome of this fusA1 mutant (EMC1) with the P. aeruginosa PAO1-derived progenitor strain (EMC0) and complemented mutant strain expressing the wild-type fusA1 gene in trans (EMC1*).
2020-09-16 | PXD017266 | Pride
Project description:Primary objectives: The study investigates whether a Escherichia coli Nissle-suspenison has a (preventive) antidiarrheal effect in patients with tumors who are treated with chemotherapeutic schemes which are associated with increased occurances of diarrhea. Diarrhea caused by treatment are thought to be reduced in intensity and/or frequency by the treatment with Escherichia coli Nissle-Suspension.
Primary endpoints: Common toxicity criteria (CTC) for diarrhea
| 2534265 | ecrin-mdr-crc
Project description:New and rapid antimicrobial susceptibility/resistance testing methods are required for bacteria from positive blood cultures. In the current study we developed and evaluated a targeted LC-MS/MS assay for the detection of beta-lactam, aminoglycoside and fluoroquinolone resistance mechanisms in blood cultures positive for E. coli or K. pneumoniae. Selected targets were the beta-lactamases SHV, TEM, OXA-1-like, CTX-M-1-like, CMY-2-like, chromosomal E. coli AmpC, OXA-48-like, NDM, VIM and KPC, the aminoglycoside modifying enzymes AAC(3)-Ia, AAC(3)-II, AAC(3)-IV, AAC(3)-VI, AAC(6’)-Ib, ANT(2”)-I and APH(3’)-VI, the 16S-RMTases ArmA, RmtB, RmtC and RmtF, the quinolone resistance mechanisms QnrA, QnrB, AAC(6’)-Ib-cr, the wildtype QRDR of GyrA, and for E. coli, the porins OmpC and OmpF. The developed assay was evaluated using 100 prospectively collected positive blood cultures, 100 negative blood cultures inoculated with isolates that were previously collected from blood cultures, and 48 isolates inoculated with isolates carrying genes of less prevalent resistance mechanisms.
2022-07-01 | PXD025365 | Pride
Project description:Evolution of antibiotic resistance in microbes is frequently achieved by acquisition of spontaneous mutations during antimicrobial therapy. Here we demonstrate that inactivation of a central regulator of iron homeostasis (fur) facilitates laboratory evolution of ciprofloxacin resistance in Escherichia coli. To decipher the underlying molecular mechanisms, we first performed a global transcriptome analysis and demonstrated a substantial reorganization of the Fur regulon in response to antibiotic treatment. We hypothesized that the impact of Fur on evolvability under antibiotic pressure is due to the elevated intracellular concentration of free iron and the consequent enhancement of oxidative damage-induced mutagenesis. In agreement with expectations, over-expression of iron storage proteins, inhibition of iron transport, or anaerobic conditions drastically suppressed the evolution of resistance, while inhibition of the SOS response-mediated mutagenesis had no such effect in fur deficient population. In sum, our work revealed the central role of iron metabolism in de novo evolution of antibiotic resistance, a pattern that could influence the development of novel antimicrobial strategies. We used microarrays to identify genotype specific transcriptional changes under severe DNA damaging conditions (antibiotic ciprofloxacin). We treated Escherichia coli cells with a highly toxic level of ciprofloxacin (gyrase inhibitor) for RNA extraction and hybridization on Affymetrix microarrays. We planned to find genotype specific transcriptional responses using WT control (BW25113) and fur-knockout mutant (selected from the KEIO collection) strains during antibiotic treatments. For each treatment type we used two biological replicates.
2014-09-11 | E-GEOD-55662 | biostudies-arrayexpress
Project description:The purpose of this study is to determine whether the presence of pathogenic Escherichia coli in colon is associated with psychiatric disorders.
| 2230352 | ecrin-mdr-crc
Project description:To demonstrate plasmid transferability by conjugation, cultures of the donor S. Infantis, and recipient Escherichia coli (E. coli) K12 were mated. S. Infantis and transconjugant were screened for resistance genes.
2016-01-12 | E-MTAB-4108 | biostudies-arrayexpress