Burkholderia pseudomallei transcriptional adaptation in macrophage
Ontology highlight
ABSTRACT:
ORGANISM(S): Burkholderia pseudomallei Burkholderia pseudomallei K96243
PROVIDER: GSE27558 | GEO | 2011/12/31
SECONDARY ACCESSION(S): PRJNA138393
REPOSITORIES: GEO
Similar Datasets
Project description:This study reports the expression profile of intracellular B. pseudomallei following infection of human macrophage-like U937 cells. The transcriptome of intracellular B. pseudomallei harvested from macrophage cells over an infection period of 6 hr (1, 2, 4 and 6 hr post-infection) were compared to in vitro grown bacteria to identify genes whose expression is altered in response to intracellular growth. The experimental design of this study involved the total RNA from intracellular B. pseudomallei harvested from infected U937 cells at 4 selected time points with 3 biological replicates each. The microarray data from each time point was compared relative to in vitro grown bacteria in cell culture medium.
2011-12-31 | E-GEOD-27558 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse macrophage cells comparing control untreated cells with macrophage cells infected with Burkeholderia pseudomallei. Goal was to determine the effects of bacterial infection on global macrophage gene expression.
2011-07-15 | GSE30642 | GEO
Project description:Transcriptional profiling of mouse macrophage cells comparing control untreated cells with macrophage cells infected with Burkeholderia pseudomallei. Goal was to determine the effects of bacterial infection on global macrophage gene expression. Two-condition experiment, macrophage vs. infected macrophage cells.
2011-07-14 | E-GEOD-30642 | biostudies-arrayexpress
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
2024-03-06 | GSE244127 | GEO
Project description:The potential for epigenetic changes in host cells following microbial infection has been widely suggested, but few examples have been reported. We assessed genome-wide patterns of DNA methylation in human macrophage-like U937 cells following infection with Burkholderia pseudomallei, an intracellular bacterial pathogen and the causative agent of human melioidosis. Our analyses revealed significant changes in host cell DNA methylation, at multiple CpG sites in the host cell genome, following infection. Infection induced differentially methylated probes (iDMPs) showing the greatest changes in DNA methylation were found to be in the vicinity of genes involved in inflammatory responses, intracellular signalling, apoptosis and pathogen-induced signalling. A comparison of our data with reported methylome changes in cells infected with M. tuberculosis revealed commonality of differentially methylated genes, including genes involved in T cell responses (BCL11B, FOXO1, KIF13B, PAWR, SOX4, SYK), actin cytoskeleton organisation (ACTR3, CDC42BPA, DTNBP1, FERMT2, PRKCZ, RAC1), and cytokine production (FOXP1, IRF8, MR1). Overall our findings show that pathogenic-specific and pathogen-common changes in the methylome occur following infection.
2016-06-16 | GSE83379 | GEO
Project description:The potential for epigenetic changes in host cells following microbial infection has been widely suggested, but few examples have been reported. We assessed genome-wide patterns of DNA methylation in human macrophage-like U937 cells following infection with Burkholderia pseudomallei, an intracellular bacterial pathogen and the causative agent of human melioidosis. Our analyses revealed significant changes in host cell DNA methylation, at multiple CpG sites in the host cell genome, following infection. Infection induced differentially methylated probes (iDMPs) showing the greatest changes in DNA methylation were found to be in the vicinity of genes involved in inflammatory responses, intracellular signalling, apoptosis and pathogen-induced signalling. A comparison of our data with reported methylome changes in cells infected with M. tuberculosis revealed commonality of differentially methylated genes, including genes involved in T cell responses (BCL11B, FOXO1, KIF13B, PAWR, SOX4, SYK), actin cytoskeleton organisation (ACTR3, CDC42BPA, DTNBP1, FERMT2, PRKCZ, RAC1), and cytokine production (FOXP1, IRF8, MR1). Overall our findings show that pathogenic-specific and pathogen-common changes in the methylome occur following infection. The human leukemic monocyte lymphoma cell line (U937, ATCC CRL-1593.2) was maintained in RPMI 1640 supplemented with 10% foetal bovine serum (FBS) at 37°C. U937 cells were differentiated to macrophage-like cells following exposure to 20 ng/ml (final concentration) of phorbol 12-myristate 13-acetate (PMA) for 48 hours at 37°C and differentiation evidenced by increased adherence to tissue culture flasks. Overnight cultures of B. pseudomallei K96243 were diluted in L-15 medium and added to differentiated U937 cells at a multiplicity of infection (MOI) of 10. Uninfected controls were overlaid with L15 medium only. The cells were then incubated at 37°C to allow infection. The cells were washed 3 times with PBS and incubated with fresh L15 medium containing 1mg/ml kanamycin to kill extracellular bacteria. At appropriate time points the cells were washed 3 times in warm PBS and lysed with 0.1% (vol/vol) Triton X-100. DNA was isolated using an AllPrep kit (Qiagen) and stored at -80ºC until required. DNA yield was measured using a Nanodrop instrument with measurements between 22.8 â 50.6 ng/ul. Two experiments were carried out using the above procedure. In Experiment 1, DNA was collected from uninfected and infected cells at 2 hours (T2), and 4 hours (T4) post infection (2 biological replicates and 2 technical replicates from each group). In Experiment 2, DNA was collected from uninfected and infected cells at 1 hour (T1), 2 hours (T2), 3 hours (T3) and 4 hours (T4) post infection (1 sample from each group). The DNA methylation profile was determined using the Infinium HumanMethylation450 BeadChip (450K) (Illumina Inc.) following the manufacturerâs instructions. The data was extracted and the initial analysis was performed using GenomeStudio (2010.3) methylation module (1.8.5). Quality control checks and quantile normalisation were implemented using WateRmelon. Samples with more than 1% of sites with a detection p-value greater than 0.05 were removed as were probes with 1% of samples with a detection p-value greater than 0.05. Probes were removed if they had a bead count less than 3 in 1% of samples. Cross-hybridizing probes were removed, leaving 425496 probes for analysis. Here we report DNA methylation profile of 18 samples (10 infected and 8 control).
2016-06-16 | E-GEOD-83379 | biostudies-arrayexpress
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.
2013-09-12 | GSE43205 | GEO
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 M-bM-^@M-^S a so-called M-bM-^@M-^\condition compendiumM-bM-^@M-^]. 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. The transcriptome profiles of Bp exposed to 82 conditions were captured using a custom-designed tiling microarray and compiled into a compendium revealing novel genomic features and co-expression network.
2013-09-12 | E-GEOD-43205 | biostudies-arrayexpress
Project description:Burkholderia pseudomallei transcriptional adaptation in macrophage
| PRJNA138393 | ENA
Project description:Burkholderia pseudomallei is the causative agent of melioidosis which is endemic to Southeast Asia and Northern Australia. It is a Gram-negative soil and water bacterium that represents a potential bioterrorism threat. Colony morphology variation is a remarkable feature in primary clinical cultures of B. pseudomallei. Differences in expression of several potential virulence and survival genes were believed to be associated with B. pseudomallei colony morphology variants. Microarrray approach was used to investigate alterations of the global B. pseudomallei transcriptome profile at the mid-logarithmic phase of growth, among the wild type (WT) and small colony variant (SCV) of B. pseudomallei pre- and post-exposed to human lung epithelial cells, A549. Generally, SCV pre- and post-exposed have lower metabolic requirements and consume lesser energy than WT pre- and post-exposed to A549; however, both WT and SCV may limit their metabolic activity during the infection of A549 cells and this is indicated by the down-regulation of genes implicated in metabolism of amino acids, carbohydrate, lipid, and other amino acids, and biodegradation of xenobiotics. On the other hand, many well-known virulence and survival factors including T3SS, T6SS, fimbriae, capsular polysaccharides, drug resistance and stress response were up-regulated in both WT and SCV pre- and post-exposed to A549 cells. Several virulence factors expressed at the mid-logarithmic phase of growth. Microarray analysis on the different morphotypes demonstrated the essential difference in bacterial response associated with virulence and survival pre- and post-exposed to A549 cells.
2016-10-12 | GSE87827 | GEO