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Burkholderia pseudomallei

ABSTRACT: Burkholderia pseudomallei - Maryland Aquarium 2019

PROVIDER: PRJNA760327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16343583_1.fastq.gz	Fastqsanger.gz
	SRR16343583_2.fastq.gz	Fastqsanger.gz
	SRR16343584_1.fastq.gz	Fastqsanger.gz
	SRR16343584_2.fastq.gz	Fastqsanger.gz
	SRR16343585_1.fastq.gz	Fastqsanger.gz

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Methylome sequencing of Burkholderia pseudomallei strains Bp33 and Bp35

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Role of ppiB in burkholderia pseudomallei

Project description:Burkholderia pseudomallei is the causative agent of melioidosis a disease endemic in South-East Asia and Northern Australia. The mortality rates in these areas are unacceptably high even with antibiotic treatment, attributed to intrinsic and acquired resistance of B. pseudomallei to antibiotics. With very few options for therapeutics there is an urgent requirement to identify anti-bacterial targets for the development of novel, effective treatments. In this study we examine the role and effect of ppiB on the proteome. Using LFQ analysis we show loss of ppiB has dramatic effect on the Burkholderia pseudomallei proteome.

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Effect of Mip inhibition on J774A.1 macrophage immune response during Burkholderia pseudomallei infection

Project description:Melioidosis, caused by the Gram-negative bacterium Burkholderia pseudomallei, is a disease endemic to South-East Asia and Northern Australia. Clinical presentation is highly variable, ranging from asymptomatic to fatal septicaemia, and thus the outcome of infection can depend on the host immune responses. The aim of this study was to characterise the macrophage immune response to B. pseudomallei in the presence of novel inhibitors targeting the virulence factor, Macrophage Infectivity Potentiator (Mip) protein. To do this. murine macrophage J774A.1 cells were infected with B. pseudomallei K96243 in the presence and absence of two small-molecule inhibitors designed to target the Mip protein. Global transcriptional profiling of macrophages infected with B. pseudomallei was analysed by RNA-Seq four hours post-infection. In the presence of Mip inhibitors, we found a significant reduction in the expression of pro-inflammatory cytokines highlighting the potential to utilize Mip inhibitors to dampen potentially harmful pro-inflammatory responses resulting from B. pseudomallei infection in macrophages. We then performed gene expression profiling analysis using data obtained from RNA-seq of J774A.1 macrophages infected with Burkholderia pseudomallei in the presence of two Mip inhibitors or vehicle control 4 hours post-infection

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Project description:Bacterial transcriptomes are dynamic, context-specific and condition-dependent. Infection by the soil bacterium, Burkholderia pseudomallei, causes melioidosis, an often fatal infectious disease of humans and animals. Possessing a large multi-chromosomal genome, B. pseudomallei is able to persist and survive in a multitude of environments. To obtain a comprehensive overview of B. pseudomallei expressed transcripts, we initiated whole-genome transcriptome profiling covering a broad spectrum of conditions and exposures – a so-called “condition compendium”. Using the compendium, we confirmed many previously-annotated genes and operons, and also identified hundreds of novel transcripts including anti-sense transcripts and non-coding RNAs. By systematically examining genes exhibiting highly similar expression patterns, we ascribed putative functions to previously uncharacterized genes, and identified novel regulatory elements controlling these expression patterns. We also used the compendium to elucidate candidate virulence pathways associated with quorum-sensing and infection in mice. Our study showcases the power of a B. pseudomallei condition compendium as a valuable resource for understanding microbial physiology and the pathogenesis of melioidosis.

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Transcriptomics analysis during the transient ceftazidime tolerance of Burkholderia pseudomallei

Project description:B. pseudomallei strain K96243 is sensitive to the drug ceftazidime (CAZ), but has been shown to exhibit transient CAZ tolerance when in a biofilm form. To investigate an observed shift in gene expression profile during ceftazidime (CAZ) tolerance and to better understand the mechanistic aspects of this transient tolerance, RNA-sequencing was performed on B. pseudomallei K96243 from the following three growth states: planktonic-free, biofilm, and planktonic shedding cells. Results indicated that the expression of 651 genes (10.97%) were significantly changed in both biofilm (resistant) and planktonic shedding (sensitive) cells in comparison to the planktonic state. Burkholderia biofilm shifts its transcriptome in response to ceftazidime exposure by regulating iron-sulfur stabilizing and metabolic-related genes.

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