Ontology highlight
ABSTRACT:
PROVIDER: PRJNA884167 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21707200_1.fastq.gz | Fastqsanger.gz | |||
| SRR21707200_2.fastq.gz | Fastqsanger.gz | |||
| SRR21707201_1.fastq.gz | Fastqsanger.gz | |||
| SRR21707201_2.fastq.gz | Fastqsanger.gz | |||
| SRR21707202_1.fastq.gz | Fastqsanger.gz |
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Project description:Bacterial phenotypic flexibility on phage-bacterial coevolution- Bacterial sequencing data
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Project description:Antibiotic use can lead to expansion of multi-drug resistant pathobionts within the gut microbiome that can cause life-threatening infections. Selective alternatives to conventional antibiotics are in dire need. Here, we describe a Klebsiella PhageBank that enables the rapid design of antimicrobial bacteriophage cocktails to treat multi-drug resistant Klebsiella pneumoniae. Using a transposon library in carbapenem-resistant K. pneumoniae, we identified host factors required for phage infection in major Klebsiella phage families. Leveraging the diversity of the PhageBank and experimental evolution strategies, we formulated combinations of phages that minimize the occurrence of phage resistance in vitro. Optimized bacteriophage cocktails selectively suppressed the burden of multi-drug resistant K. pneumoniae in the mouse gut microbiome and drove bacterial populations to lose key virulence factors that act as phage receptors. Further, phage-mediated diversification of bacterial populations in the gut enabled co-evolution of phage variants with higher virulence and a broader host range. Altogether, the Klebsiella PhageBank represents a roadmap for both phage researchers and clinicians to enable phage therapy against a critical multidrug-resistant human pathogen.
2024-10-01 | GSE272297 | GEO
Project description:Endolysins are peptidoglycan hydrolases produced at the end of the bacteriophage (phage) replication cycle to lyse the host cell. Gram-positive phages endolysins come in a variety of multi-modular forms that combine different catalytic domains and may have evolved to adapt to their bacterial hosts. However, the reason why phage can adopt endolysin with such complex multidomain architecture is for the moment not well understood. We used the Streptococcus dysgalactiae phage endolysin PlySK1249 as a model to study the implication of multi-domain architecture in phage-induced bacterial lysis and lysis regulation. The activity of the enzyme relied on a bacteriolytic amidase (Ami), a non-bacteriolytic L-Ala-D-Ala endopeptidase (CHAP) acting as a de-chaining enzyme and central LysM cell wall binding domain (CBD). Ami and CHAP synergized for peptidoglycan digestion and bacteriolysis in the native enzyme or when expressed individually and reunified in vitro. This cooperation could be modulated by bacterial cell wall-associated proteases, which specifically cleaved the two linkers connecting the different domains. While both catalytic domains were observed to act coordinately to optimize bacterial lysis, the CBD is expected to delay diffusion of the enzyme until proteolytic inactivation is achieved. As for certain autolysins, PlySK1249 cleavage by bacterial cell wall associated proteases might be an example of dual phage-bacterial regulation and mutual coevolution.
2021-04-15 | PXD024020 | Pride
Project description:RNA sequencing (RNA-seq) of phage infected bacterial cultures offers a snapshot of transcriptional events occurring during the infection process, providing insights into the phage transcriptional organization as well as the bacterial response. To better mimic real environmental contexts, we performed RNA-seq of P. aeruginosa PAO1 cultures infected with phage LUZ19 in a mammalian cell culture medium (MCCM) to better simulate a phage therapy event, and the data were compared to LB medium. Regardless of the media, phage LUZ19 induces significant transcriptional changes in the bacterial host over time, particularly during early infection (t= 5 min) and gradually shuts down bacterial transcription. In a common response in both media, 56 P. aeruginosa PAO1 genes are differentially transcribed and clustered into several functional categories such as metabolism, translation and transcription. Our data allowed us to tease apart a medium-specific response during infection from the identified infection-associated responses. This reinforces the concept that phages overtake bacterial transcriptome in a strict manner to gain control of the bacterial machinery and reallocate resources for infection, in this case overcoming the nutritional limitations of the mammalian cell culture medium. From a phage therapy perspective, this study contributes towards a better understanding of phage-host interaction in human physiological conditions and demonstrates the versatility of phage LUZ19 to adapt to different environments.
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Project description:Enterococcal-phage coevolution
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Project description:Phage therapy is a promising adjunct therapeutic approach against bacterial multidrug-resistant infections, including Pseudomonas aeruginosa-derived infections. Nevertheless, the current knowledge about the phage-bacteria interaction within a human environment is limited. In this work, we performed a transcriptome analysis of phage-infected P. aeruginosa adhered to a human epithelium (Nuli-1 ATCC® CRL-4011™). To this end, we performed RNA-sequencing from a complex mixture comprising phage–bacteria–human cells at early, middle, and late infection and compared it to uninfected adhered bacteria. Overall, we demonstrated that phage genome transcription is unaltered by bacterial growth and phage employs a core strategy of predation through upregulation of prophage-associated genes, a shutdown of bacterial surface receptors, and motility inhibition. In addition, specific responses were captured under lung-simulating conditions, with the expression of genes related to spermidine syntheses, sulfate acquisition, spermidine syntheses, biofilm formation (both alginate and polysaccharide syntheses), lipopolysaccharide (LPS) modification, pyochelin expression, and downregulation of virulence regulators. These responses should be carefully studied in detail to better discern phage-induced changes from bacterial responses against phage. Our results establish the relevance of using complex settings that mimics in vivo conditions to study phage-bacteria interplay, being obvious the phage versatility on bacterial cell invasion.
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Project description:Clinical case studies have reported that the combined use of specific lytic phage(s) and antibiotics reduces the severity of difficult-to-treat Pseudomonas aeruginosa infections in many patients. In vitro methods that attempt to reproduce specific pathophysiological conditions can provide a reliable assessment of the antibacterial effects of phages. Here, we measured bacterial killing kinetics and individual phage replication in different growth phases, including biofilms, elucidating factors influencing the efficacy of two phages against the laboratory strain P. aeruginosa PAO1. While two-phage combination treatment effectively eliminated P. aeruginosa in routine broth and in infected human lung cell cultures, the emergence of phage-resistant variants occurred under both conditions. Phage combination displayed initial inhibition of biofilm dispersal, but sustained control was achieved only with a combination of phages and meropenem. In contrast, surface-attached biofilm exhibited tolerance to phage and/or meropenem, suggesting a spatiotemporal variation in antibacterial effect. Moreover, the phage with the shorter lysis time killed P. aeruginosa more rapidly, selecting a specific nucleotide polymorphism that likely conferred a competitive disadvantage and cross resistance to the second phage of the combination. These findings highlight biofilm developmental phase, inter-phage competition and phage resistance as factors limiting the in vitro efficacy of a phage combination. However, their precise impact on the outcome of phage therapy remains uncertain, necessitating validation through phage efficacy trials in order to establish clearer correlations between laboratory assessments and clinical results.
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