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Burkholderia pseudomallei K96243

ABSTRACT: Burkholderia pseudomallei K96243 Genome sequencing

PROVIDER: PRJNA235893 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR1614021_1.fastq.gz	Fastqsanger.gz
	SRR1614021_2.fastq.gz	Fastqsanger.gz
	SRR1614022.fastq.gz	Fastqsanger.gz
	SRR1614022_1.fastq.gz	Fastqsanger.gz

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Burkholderia pseudomallei K96243

Project description:Burkholderia pseudomallei K96243 re-sequencing

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B. pseudomallei K96243 genome: Control vs. B. pseudomallei environmental or clinical isolates

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B. pseudomallei K96243 genome: Control vs. B. pseudomallei environmental or clinical isolates

Project description:To use whole genome microarrays to compare the differences in genome contents of 5 B. pseudomallei isolated from clinical specimens and environmental sample with B. pseudomallei K96243 reference strain and reveals variable patterns of Genomic Islands (GIs) Keywords: Comparative genomic hybridization DNA microarrays were used to compare genome of clinical and environmental B. pseudomallei isolates with B. pseudomallei K96243 reference strain (B. pseudomallei K96243 vs. B. pseudmallei isolates). Each hybridization was used for comparison between B. pseudomallei K96243 as a reference strain with environmental isolate BP45s, environmental isolate BP28L, clinical isolate H307, clinical isolate P54, clinical isolate P82. Two replicate per array. Multiple hits with 90-99.99 % identity correspond to other locus are replicate of their genes were averaged and analyzed.

2012-07-30 | E-GEOD-19558 | biostudies-arrayexpress

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.

2021-06-30 | GSE168275 | GEO

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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