Paundecimvirus
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB17572 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Antimicrobial peptides (AMPs) are garnering attention as possible alternatives to antibiotics. Here, we describe the antimicrobial properties of epinecidin-1 against multi-drug resistant clinical isolates of P. aeruginosa (P. aeruginosa (R)) and P. aeruginosa from ATCC (P. aeruginosa (19660)) in vivo. The minimum inhibitory concentrations (MICs) of epinecidin-1 against P. aeruginosa (R) and P. aeruginosa (19660) were determined, and compared with those of imipenem. Epinecidin-1 was found to be highly effective at combating peritonitis infection caused by P. aeruginosa (R) or P. aeruginosa (19660) in mouse models, without inducing adverse behavioral effects, or liver or kidney toxicity. Taken together, our results indicate that epinecidin-1 enhances the survival rate of mice infected with the bacterial pathogen P. aeruginosa through both antimicrobial and immunomodulatory effects. RNA from mice treated with epinecidin-1 were individually compared to RNA from PBS control mice.
2014-05-27 | E-GEOD-57976 | biostudies-arrayexpress
Project description:Antimicrobial peptides (AMPs) are garnering attention as possible alternatives to antibiotics. Here, we describe the antimicrobial properties of epinecidin-1 against multi-drug resistant clinical isolates of P. aeruginosa (P. aeruginosa (R)) and P. aeruginosa from ATCC (P. aeruginosa (19660)) in vivo. The minimum inhibitory concentrations (MICs) of epinecidin-1 against P. aeruginosa (R) and P. aeruginosa (19660) were determined, and compared with those of imipenem. Epinecidin-1 was found to be highly effective at combating peritonitis infection caused by P. aeruginosa (R) or P. aeruginosa (19660) in mouse models, without inducing adverse behavioral effects, or liver or kidney toxicity. Taken together, our results indicate that epinecidin-1 enhances the survival rate of mice infected with the bacterial pathogen P. aeruginosa through both antimicrobial and immunomodulatory effects.
2014-05-27 | GSE57976 | GEO
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:Draft Genome Sequences of Pesudomonas species causing Otitis externa infection
| PRJNA695104 | ENA
Project description:Biofilms are surface-adhered bacterial communities encased in an extracellular matrix composed of polysaccharides, proteins, and extracelluar (e)DNA, with eDNA being required for the formation and integrity of biofilms. Here we demonstrate that the spatial and temporal release of eDNA is regulated by BfmR, a regulator essential for Pseudomonas aeruginosa biofilm development. The expression of bfmR coincided with localized cell death and DNA release, with high eDNA concentrations localized to the outer part of microcolonies in the form of a ring and as a cap on small clusters. Additionally, eDNA release and cell lysis increased significantly following bfmR inactivation. Genome-wide transcriptional profiling indicated that bfmR was required for repression of genes associated with bacteriophage assembly and bacteriophage-mediated lysis. In order to determine which of these genes were directly regulated by BfmR, we utilized chromatin immunoprecipitation (ChIP) analysis to identify the promoter of PA0691, termed here phdA, encoding a previously undescribed homologue of the prevent-host-death (Phd) family of proteins. Lack of phdA expression coincided with impaired biofilm development, increased cell death and bacteriophage release, a phenotype comparable to ΔbfmR. Expression of phdA in ΔbfmR biofilms restored eDNA release, cell lysis, release of bacteriophages, and biofilm formation to wild type levels. Moreover, overexpression of phdA rendered P. aeruginosa resistant to lysis mediated by superinfective bacteriophage Pf4 which was only detected in biofilms. The expression of bfmR was stimulated by conditions resulting in membrane perturbation and cell lysis. Thus, we propose that BfmR regulates biofilm development by controlling bacteriophage-mediated lysis and thus, cell death and eDNA release, via PhdA. For biofilm growth experiments, three independent replicates of P. aeruginosa strains PAO1 and ΔbfmR were grown as biofilms in a flow-through system using a once-through continuous flow tube reactor system for biofilm sample collection and in flow cells (BioSurface Technologies) for the analysis of biofilm architecture as previously described (Sauer et al., 2002, Sauer et al., 2004, Petrova & Sauer, 2009). Cells were treated with RNAprotect (Qiagen), and total RNA was extracted using an RNeasy mini purification kit (Qiagen) per the manufacturer’s instructions. RNA quality and the presence of residual DNA were checked on an Agilent Bioanalyzer 2100 electrophoretic system pre- and post-DNase treatment. Ten micrograms of total RNA was used for cDNA synthesis, fragmentation, and labeling according to the Affymetrix GeneChip P. aeruginosa genome array expression analysis protocol. Sauer, K., A. K. Camper, G. D. Ehrlich, J. W. Costerton & D. G. Davies, (2002) Pseudomonas aeruginosa displays multiple phenotypes during development as a biofilm. J. Bacteriol. 184: 1140-1154. Sauer, K., M. C. Cullen, A. H. Rickard, L. A. H. Zeef, D. G. Davies & P. Gilbert, (2004) Characterization of nutrient-induced dispersion in Pseudomonas aeruginosa PAO1 biofilm. J. Bacteriol. 186: 7312-7326. Petrova, O. E. & K. Sauer, (2009) A novel signaling network essential for regulating Pseudomonas aeruginosa biofilm development. PLoS Pathogens 5: e1000668.
2011-06-01 | E-GEOD-28953 | biostudies-arrayexpress
Project description:Bacteriophage infectivity against Pseudomonas aeruginosa in simulated saline conditions
| PRJEB23782 | ENA
Project description:Cancer cell line panels that incorporate genomic and pharmacologic screening data have become powerful tools for investigating the relationship between gene expression and drug response in human cancer research. Similar cell line panels of such a scale as the NCI60, CCLE, or GDSC do not currently exist in canine cancer research. Here we have assembled a canine cancer cell line panel of 29 cell lines representing multiple tumor types that have undergone gene expression profiling and have begun to be used for pharmacologic screening. RNA was extracted from drug naïve canine cancer cell lines and subjected to microarray analysis.
2015-12-18 | E-GEOD-76126 | biostudies-arrayexpress