RNA-seq analyzes the effect of ptsI on transcriptome in Escherichia coli during ciprofloxacin treatment.
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ABSTRACT:
PROVIDER: PRJNA551458 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13601449_1.fastq.gz | Fastqsanger.gz | |||
| SRR13601449_2.fastq.gz | Fastqsanger.gz | |||
| SRR13601450_1.fastq.gz | Fastqsanger.gz | |||
| SRR13601450_2.fastq.gz | Fastqsanger.gz | |||
| SRR13601451_1.fastq.gz | Fastqsanger.gz |
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Project description:RNA-seq analyzes the effect of purA on transcriptome in Escherichia coli during ciprofloxacin treatment.
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Project description:PurA encodes an adenylosuccinate synthetase that catalyzes the first step in the de novo synthesis of AMP. A deficiency in purA has been found to confer Escherichia coli tolerance to diverse types of antibiotics. To understand the molecular basis of the increased tolerance, we performed RNA-seq analysis to compare the transcriptional profiles of wild-type and ΔpurA mutant strains before and after ciprofloxacin treatment. The data showed that the purA deficiency suppresses transcript levels from NADH:quinone oxidoreductase genes prior to stress exposure, thereby predisposing E. coli to antibiotic tolerance by reducing respiration. During ciprofloxacin exposure, a purA deficiency suppressed a surge in expression of TCA cycle and ATP synthesis genes and the accumulation of intracellular ATP and ROS, thereby conferring bacterial tolerance to diverse antibiotic stresses.
2025-03-25 | GSE292923 | GEO
Project description:A deficiency in ptsI, encoding a cytoplasmic protein that serves as the gateway for the phosphoenolpyruvate:sugar phosphotransferase system, was found to confer tolerance to diverse types of disinfectants and antimicrobials. To understand the molecular basis of the increased tolerance, we performed RNA-seq analysis to compare the transcriptional profiles of the wild-type and the ΔptsI mutant strains before and after ciprofloxacin treatment. The data showed that cirpofloxacin treatment drastically increased the exprerssion of genes encoding enzymes in the TCA cycle and that the ptsI mutation suppressed the expression of most TCA genes and all ATP synthase genes, but elevated some of the genes involved in glycolysis and the pentose phosphate pathway (PPP) genes. Such transcriptomic alteration reduced stress-induced surge in respiration and accumutaion of toxic reaactive oxygen species, thereby conferring bacterial tolerance to diverse lethal stressors.
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Project description:Kaiser2014 - Salmonella persistence after ciprofloxacin treatment
The model describes the bacterial tolerance to antibiotics. Using a mouse model for Salmonella diarrhea, the authors have found that bacterial persistence occurs in the presence of the antibiotic ciprofloxacin because Salmonella can exist in two different states. One, the fast-growing population that spreads in the host's tissues and the other, slow-growing "persister" population that hide out inside dendritic cells of the host's immune system and cannot be attacked by the antibiotics. However, this can be killed by adding agents that directly stimulate the host's immune defense.
This model is described in the article:
Cecum lymph node dendritic cells harbor slow-growing bacteria phenotypically tolerant to antibiotic treatment.
Kaiser P, Regoes RR, Dolowschiak T, Wotzka SY, Lengefeld J, Slack E, Grant AJ, Ackermann M, Hardt WD.
PLoS Biol. 2014 Feb 18;12(2):e1001793.
Abstract:
In vivo, antibiotics are often much less efficient than ex vivo and relapses can occur. The reasons for poor in vivo activity are still not completely understood. We have studied the fluoroquinolone antibiotic ciprofloxacin in an animal model for complicated Salmonellosis. High-dose ciprofloxacin treatment efficiently reduced pathogen loads in feces and most organs. However, the cecum draining lymph node (cLN), the gut tissue, and the spleen retained surviving bacteria. In cLN, approximately 10%-20% of the bacteria remained viable. These phenotypically tolerant bacteria lodged mostly within CD103⁺CX₃CR1⁻CD11c⁺ dendritic cells, remained genetically susceptible to ciprofloxacin, were sufficient to reinitiate infection after the end of the therapy, and displayed an extremely slow growth rate, as shown by mathematical analysis of infections with mixed inocula and segregative plasmid experiments. The slow growth was sufficient to explain recalcitrance to antibiotics treatment. Therefore, slow-growing antibiotic-tolerant bacteria lodged within dendritic cells can explain poor in vivo antibiotic activity and relapse. Administration of LPS or CpG, known elicitors of innate immune defense, reduced the loads of tolerant bacteria. Thus, manipulating innate immunity may augment the in vivo activity of antibiotics.
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2024-09-02 | BIOMD0000000527 | BioModels
Project description:Microarray experiments were preformed comparing the effect of sub-inhibitory concentrations of ciprofloxacin on five independent cultures of PAO1 and the PAO1 Lon mutant
2012-03-25 | E-MTAB-1000 | biostudies-arrayexpress
Project description:Campylobacter jejuni is one of the most important zoonotic enteric bacterial pathogens able to colonize the gastrointestinal tract of various animals. The number of campylobacteriosis cases has increased worldwide and the particular concern has been the high level of fluoroquinolone resistance observed in C. jejuni isolates. In this study, we explored the effect of ciprofloxacin in Campylobacter jejuni by gene expression microarray analysis. The comparisons of transcriptional responses were performed in the absence and presence of ciprofloxacin with the wild-type strain 81-176 and its intermediate-resistant variant (P3). The resistant variant contained a single-nucleotide mutation causing amino acid change Asp-90-Asn in the gyrA gene instead of the most common Thr-86-Ile, causing a high-level resistance to ciprofloxacin. After the short-term exposure to a relatively high concentration of ciprofloxacin, the viability of C. jejuni 81-176 wild-type cells remained notably high when compared with other gram-negative bacteria. The general responses of short-term ciprofloxacin exposure were determined from both genetic backgrounds and resulted in the expression variation of genes participating in general cellular processes, e.g. , in carbon and amino-acid metabolism and protein transport. Ciprofloxacin effect for gene expression was measured from both genetic backgrounds after 1 hour exposure at the level of 0 and 8 µg/ml ciprofloxacin in MH-broth. For RNA isolation, 5 independent experiments with and without ciprofloxacin were performed, and 4 replicates of each total RNA was applied for the gene expression study.
2012-12-31 | E-GEOD-41822 | biostudies-arrayexpress
Project description:High stability of fluoroquinolone-resistant Escherichia coli in the gut during and after ciprofloxacin treatment
| PRJEB33552 | ENA
Project description:Background: Antibiotic resistance is an urgent threat to public health. Prior to the evolution of antibiotic resistance, bacteria frequently undergo response and tend to develop a state of adaption to the antibiotic. Ciprofloxacin is a broad-spectrum antibiotic by damaging DNA. With the widespread clinical application, the resistance of bacteria to ciprofloxacin continues to increase. This study aimed to investigate the transcriptome changes under the action of high concentration of ciprofloxacin in Escherichia coli. Results: We identified 773 up-regulated differentially expressed genes (DEGs) and 645 down-regulated DEGs in ciprofloxacin treated cells. Enriched biological pathways reflected the up-regulation of biological process such as DNA damage and repair system, toxin/antitoxin systems, formaldehyde detoxification system, peptide biosynthetic process and cellular protein metabolic process. With KEGG pathway analysis, up-regulated DEGs of kdsA and waa operon were associated with “LPS biosynthesis”. rfbABC operon was related to “streptomycin biosynthesis” and “polyketide sugar unit biosynthesis ”. Down-regulated DEGs of thrABC and fliL operons were associated with “flagellum-dependent cell motility” and “bacterial-type flagellum” in GO terms, and enriched into “biosynthesis of amino acids” and “flagellar assembly” in KEGG pathways. After treatment of ciprofloxacin, bacterial lipopolysacchride (LPS) release was increased by two times, and the mRNA expression level of LPS synthesis genes, waaB, waaP and waaG were elevated (P < 0.05). Conclusions: Characterization of the gene clusters by RNA-seq showed high dose of ciprofloxacin not only lead to damage of bacterial macromolecules and components, but also induce protective response against antibiotic action by up-regulating the SOS system, toxin/antitoxin system and formaldehyde detoxification system. Moreover, genes related to biosynthesis of LPS were also upregulated by the treatment indicating that ciprofloxacin can enhance the production of endotoxin on the level of transcription. These results demonstrated that transient exposure of high dose ciprofloxacin is double edged. Cautions should be taken when administering the high dose antibiotic treatment for infectious diseases.
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Project description:comparison of total RNA profiles obtained from ciprofloxacin resistant colonies of two separate Enteritidis isolates with their respective wt parents
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Project description:Transcriptional profiling of S. coelicolor comparing control untreated cells with ciprofloxacin treated cells. Two-condition experiment, Control Vs CIP treatment. Biological replicates: 3 control, One dye swap replicate. four samples and three biological replicate to study the response of S. coleicolor cells to ciprofloxacin
2014-01-01 | E-GEOD-49788 | biostudies-arrayexpress