Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30991 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3097840_1.fastq.gz | Fastqsanger.gz | |||
| ERR3097840_2.fastq.gz | Fastqsanger.gz | |||
| ERR3097850_1.fastq.gz | Fastqsanger.gz | |||
| ERR3097850_2.fastq.gz | Fastqsanger.gz | |||
| ERR3097860_1.fastq.gz | Fastqsanger.gz |
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Project description:The emergence of polymyxin resistance in carbapenem-resistant and extended-spectrum -lactamase (ESBL)-producing bacteria is a critical 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 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 the less-toxic next-generation polymyxin derivative, FADDI-287. We were unable to select for mutants resistant to PBT2 + FADDI-287 in polymyxin resistant E. coli containing a plasmid-borne mcr-1 gene or K. pneumoniae carrying a chromosomal mgrB mutation. Using a highly invasive K. pneumoniae strain engineered for polymyxin resistance through mgrB mutation, we successfully demonstrated the efficacy of PBT2 + FADDI-287 in vivo for the treatment of Gram-negative sepsis. These data present a new treatment modality to break antibiotic resistance in high priority polymyxin-resistant Gram-negative pathogens.
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Project description:An M307 G/A point mutation of FUT1 gene has been considered as a usful marker to select the piglets that are sensitive(GG/AG genotype) or resistant(AA) to Escherichia coli F18 in foreign pig breeds. However,it is not suitable to Chinese native breeds. Duodenal tissues were collected from 3 full-sib pairs of Sutai pigs (a new hybrid between the Duroc and Taihu breeds) at the age of 28-day differing in adhesion phenotype to find the differential miRNAs that can provide the basis for analyzing the different mechanisms of E.coli F18 resistance between foreign and Chinese native breeds,as well as for breeding for disease resistance in Chinese native breeds in the future. piglets at the age of 28-day sensitive(GG genotype) to Escherichia coli F18 vs resistant(AA) ones.Biological replicates:3 full-sib pairs of Sutai pigs(3 pairs for GG/AA genotype of FUT1 gene).One GG sample (512 piglet) was sequenced twice to verify the result. 2385 piglet and 2383 piglet were a pair of full-sib with AA and GG genotype at M307 positionof FUT1 gene, respectively. Unfortunately, the sequencing of 2385 was a failure and was excluded. 2385 piglet has an AA genotype of the FUT1 gene
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Project description:An M307 G/A point mutation of FUT1 gene has been considered as a usful marker to select the piglets that are sensitive(GG/AG genotype) or resistant(AA) to Escherichia coli F18 in foreign pig breeds. However,it is not suitable to Chinese native breeds. Duodenal tissues were collected from 3 full-sib pairs of Sutai pigs (a new hybrid between the Duroc and Taihu breeds) at the age of 28-day differing in adhesion phenotype to find the differential miRNAs that can provide the basis for analyzing the different mechanisms of E.coli F18 resistance between foreign and Chinese native breeds,as well as for breeding for disease resistance in Chinese native breeds in the future.
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Project description:An M307 G/A point mutation of FUT1 gene has been considered as a usful marker to select the piglets that are sensitive(GG/AG genotype) or resistant(AA) to Escherichia coli F18 in foreign pig breeds.However,it is not suitable to Chinese native breeds. Duodenal tissues were collected from 8 full-sib pairs of Sutai pigs (a new hybrid between the Duroc and Taihu breeds) at the age of 28-day differing in adhesion phenotype to find the differential genes that can be used as the candidate genes fit for Chinese native breeds. piglets at the age of 28-day sensitive (GG/AG genotype) to Escherichia coli F18 vs resistant(AA) ones.Biological replicates:8 full-sib pairs of Sutai pigs (4 pairs for GG/AA genotype of FUT1 gene, 4 pairs for AG/AA genotype)
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Project description:Background: It remains unclear how high-risk Escherichia coli lineages, like sequence type (ST) 131, initially adapt to carbapenem exposure in its progression to becoming carbapenem resistant. Methods: Carbapenem mutation frequency was measured in multiple subclades of extended-spectrum β-lactamase (ESBL) positive ST131 clinical isolates using a fluctuation assay followed by whole genome sequencing (WGS) characterization. Genomic, transcriptomic, and porin analyses of ST131 C2/H30Rx isolate, MB1860, under prolonged, increasing carbapenem exposure was performed using two distinct experimental evolutionary platforms to measure fast vs. slow adaptation. Results: All thirteen ESBL positive ST131 strains selected from a diverse (n=184) ST131 bacteremia cohort had detectable ertapenem (ETP) mutational frequencies with a statistically positive correlation between initial ESBL gene copy number and mutation frequency (r = 0.87, P<1e-5). WGS analysis of mutants showed initial response to ETP exposure resulted in significant increases in ESBL gene copy numbers or mutations in outer membrane porin (Omp) encoding genes in the absence of ESBL gene amplification with subclade specific adaptations. In both experimental evolutionary platforms, MB1860 responded to initial ETP exposure by increasing blaCTX-M-15 copy numbers via modular, insertion sequence 26 (IS26) mediated pseudocompound transposons (PCTns). Transposase activity driven by PCTn upregulation was a conserved expression signal in both experimental evolutionary platforms. Stable mutations in Omp encoding genes were detected only after prolonged increasing carbapenem exposure consistent with clinical observations. Conclusions: ESBL gene amplification is a conserved response to initial carbapenem exposure, especially within the high-risk ST131 C2 subclade. Targeting such amplification could assist with mitigating carbapenem resistance development.
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