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ABSTRACT: Backward collateral sensitivity can restore antibiotic susceptibility

PROVIDER: PRJNA1207050 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31904072_1.fastq.gz	Fastqsanger.gz
	SRR31904072_2.fastq.gz	Fastqsanger.gz
	SRR31904073_1.fastq.gz	Fastqsanger.gz
	SRR31904073_2.fastq.gz	Fastqsanger.gz
	SRR31904074_1.fastq.gz	Fastqsanger.gz

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Collateral sensitivity of antibiotic resistant bacteria to antimicrobial peptides

Project description:Cationic antimicrobial peptides (CAPs) are promising novel alternatives to conventional antibacterial agents, but the overlap in resistance mechanisms between small-molecule antibiotics and CAPs is unknown. Does evolution of antibiotic resistance decrease (cross-resistance) or increase (collateral sensitivity) susceptibility to CAPs? We systematically addressed this issue by studying the susceptibilities of a comprehensive set of antibiotic resistant Escherichia coli strains towards 24 antimicrobial peptides. Strikingly, antibiotic resistant bacteria frequently showed collateral sensitivity to CAPs, while cross-resistance was relatively rare. We identified clinically relevant multidrug resistance mutations that simultaneously elevate susceptibility to certain CAPs. Transcriptome and chemogenomic analysis revealed that such mutations frequently alter the lipopolysaccharide composition of the outer cell membrane and thereby increase the killing efficiency of membrane-interacting antimicrobial peptides. Furthermore, we identified CAP-antibiotic combinations that rescue the activity of existing antibiotics and slow down the evolution of resistance to antibiotics. Our work provides a proof of principle for the development of peptide based antibiotic adjuvants that enhance antibiotic action and block evolution of resistance.

2018-03-29 | GSE96706 | GEO

Escherichia coli

Project description:Collateral Sensitivity Associated with Antibiotic Resistance Plasmids

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Escherichia coli

Project description:Collateral sensitivity of antibiotic resistant bacteria to antimicrobial peptides

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Project description:Collateral sensitivity and evolutionary repeatability

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Evolutionary collateral sensitivity to pleuromutilins in vancomycin-resistant Enterococcus faecium

Project description:The rise of antibiotic resistance and decline of antibiotic discovery urgently calls for novel mechanistic understanding of pharmacological and evolutionary interactions between antibiotics and multidrug resistant bacteria to revitalize existing antibiotics. The evolutionary cross-resistance to antibiotics has received intensive attention previously. Nevertheless, whether and how bacteria develop negative responses, under the selective pressure of antibiotics by inverting the evolutionary trajectory remains unclear. Here we found an instance of collateral sensitivity, in which clinical vancomycin-resistant Enterococcus faecium (VREfm) pathogens exhibit dramatic and specific susceptibility to pleuromutilin antibiotics, decreased minimal inhibitory concentrations (MICs) from 128 µg/mL to 0.03 µg/mL. The unique trade-off between vancomycin and pleuromutilins is mediated by the epistasis between the van gene cluster and msrC encoding an ABC-F protein protecting bacterial ribosomes. We validated the efficacy of pleuromutilins in vivo through reducing colonization and promoting microbiota restoration. Our findings provide an alternative approach to inverting the selective advantage and reversing the route of vancomycin resistance evolution, and to treat VREfm associated infections.

2022-05-20 | PXD030906 | Pride

Carbon sources tune antibiotic susceptibility in Pseudomonas aeruginosa via TCA cycle control

Project description:This study examines the mechanisms underlying fumarate- and glyoxylate-mediated changes in tobraymcyin sensitivity in PAO1 cells Grant ID: NIH Grant K99 GM 118907 Grant title: Effects of Host Metabolic Variation on Antibiotic Susceptibility Funding Source: NIH NIGMS Name: Jason Yang

2016-12-20 | GSE90620 | GEO

Pseudomonas aeruginosa PA14

Project description:Experimental evolution of high levels antibiotic resistance and collateral sensitivity in Pseudomonas aeruginosa

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Phenotypic convergent evolution towards fosfomycin collateral sensitivity of Pseudomonas aeruginosa antibiotic resistant mutants

Project description:Phenotypic convergent evolution towards fosfomycin collateral sensitivity of Pseudomonas aeruginosa antibiotic resistant mutants

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Collateral Responses to Classical Cytotoxic Chemotherapies are Heterogeneous and Sensitivities are Sparse

Project description:Chemotherapy resistance is a major obstacle to curing cancer patients. Combination drug regimens have shown promise as a method to overcome resistance; however, to date only some cancers have been cured with this method. Collateral sensitivity – the phenomenon whereby resistance to one drug is co-occurrent with sensitivity to a second drug – has been gaining traction as a promising new concept to guide rational design of combination regimens. Here we evolved over 100 subclones of the Eµ-Myc; p19ARF -/- cell line to be resistant to one of four classical chemotherapy agents: doxorubicin, vincristine, paclitaxel, and cisplatin. We then surveyed collateral responses to acquisition of resistance to these agents. Although numerous collateral sensitivities have been documented for antibiotics and targeted cancer therapies, we observed only one collateral sensitivity: half of cell lines that acquired resistance to paclitaxel also acquired a collateral sensitivity to verapamil. However, we found that the mechanism of this collateral sensitivity was unrelated to the mechanism of paclitaxel resistance. Interestingly, we observed heterogeneity in the phenotypic response to acquisition of resistance to most of the drugs we tested, most notably for paclitaxel, suggesting the existence of multiple different states of resistance. Surprisingly, this phenotypic heterogeneity in paclitaxel resistant cell lines was unrelated to transcriptomic heterogeneity among those cell lines. These features of phenotypic and transcriptomic heterogeneity must be taken into account in future studies of treated tumor subclones and in design of chemotherapy combinations.

2022-03-23 | GSE166425 | GEO

Intestinal expression in murine antibiotic-induced acceleration of Type 1 diabetes

Project description:Here we asked whether the single early-life (pup day of life P5-P10) antibiotic pulse was sufficient to enhance Type-1 Diabetes (T1D) in Non Obese Diabetic (NOD) mice. Two sets of experimental samples were analyzed for changes in intestinal pathway expression using the NOD mouse model and Pulsed Antibiotic Therapy (PAT). NODPAT sought to describe the intestinal changes related to early life PAT treatment while the RESTORE experiment sought to restore an antibiotic-perturbed host and measure the intestinal expression changes over time. We provide evidence that maternal microbiota provides partial restoration of both the altered pup microbiota and its immunological phenotypes.

2018-08-19 | E-MTAB-6826 | biostudies-arrayexpress

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