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Genome-wide analysis of blood, spleen and lung expression of C57BL/6 mice subjected to Burkholderia pseudomallei infection

ABSTRACT: Melioidosis, a severe human disease caused by the bacterium Burkholderia pseudomallei, has a wide spectrum of clinical manifestations ranging from acute septicaemia to chronic localized illness or latent infection. Mice were intranasally infected with either high or low doses of B. pseudomallei to generate either acute, chronic or latent infection and host blood and tissue transcriptional profiles were generated. Acute infection was accompanied by a homogeneous signature associated with induction of multiple innate immune response pathways, such as IL10, TREM1 and IFN-signaling, largely found in both blood and tissue. The transcriptional profile in blood reflected the heterogeneity of chronic infection and quantitatively reflected the severity of disease. Comparison of these mouse blood datasets by pathway and modular analysis with the blood transcriptional signature of patients with melioidosis showed that many genes were similarly perturbed, including IL10, TREM1 and IFNsignaling, revealing the common immune response occurring in both mice and humans.

ORGANISM(S): Mus musculus

PROVIDER: GSE61106 | GEO | 2015/09/02

SECONDARY ACCESSION(S): PRJNA260250

REPOSITORIES: GEO

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Genome-wide analysis of blood, spleen and lung expression of C57BL/6 mice subjected to Burkholderia pseudomallei infection

Project description:Melioidosis, a severe human disease caused by the bacterium Burkholderia pseudomallei, has a wide spectrum of clinical manifestations ranging from acute septicaemia to chronic localized illness or latent infection. Mice were intranasally infected with either high or low doses of B. pseudomallei to generate either acute, chronic or latent infection and host blood and tissue transcriptional profiles were generated. Acute infection was accompanied by a homogeneous signature associated with induction of multiple innate immune response pathways, such as IL10, TREM1 and IFN-signaling, largely found in both blood and tissue. The transcriptional profile in blood reflected the heterogeneity of chronic infection and quantitatively reflected the severity of disease. Comparison of these mouse blood datasets by pathway and modular analysis with the blood transcriptional signature of patients with melioidosis showed that many genes were similarly perturbed, including IL10, TREM1 and IFNsignaling, revealing the common immune response occurring in both mice and humans. Total RNA obtained from isolated blood, lung and spleen of C57BL/6 mice subjected to either acute or chronic infection by Burkolderia compared to uninfected controls.

2015-09-02 | E-GEOD-61106 | biostudies-arrayexpress

Toxicogenomic Effect of Burkholderia pseudomallei in a Human Macrophage Cell (THP-1) Model of Acute Melioidosis Using Whole-genome Microarray

Project description:Gene expression profiles of human cell (THP-1) lines exposed to a novel Daboiatoxin (DbTx) isolated from Daboia russelli russelli, and specific cytokines and inflammatory pathways involved in acute infection caused by Burkholderia pseudomallei. Keywords: Melioidosis, Burkholderia pseudomallei, Daboiatoxin, Cytokines, Inflammation.

2010-05-31 | GSE7577 | GEO

Infection with Burkholderia pseudomallei – immune correlates of survival in acute melioidosis

Project description:Melioidosis is a neglected tropical disease caused by the Gram-negative bacterium Burkholderia pseudomallei. It is widespread in Southeast Asia and under-reported across tropical regions worldwide. Patients present with a range of clinical syndromes including sepsis, pneumonia and focal abscesses, with a mortality rate of 40% in hospitalized patients in Thailand. Up to two-thirds of patients with melioidosis have diabetes mellitus. In this experiment we sought to characterize pathways activated by whole killed B. pseudomallei bacteria and by three vaccine candidate proteins from B. pseudomallei, BPSL2520 (uncharacterized protein), BPSS1525 (BopE) and BPSL2096 (AhpC) in patients with diabetes and acute melioidosis.

2017-09-22 | E-MTAB-6093 | biostudies-arrayexpress

Delayed activation of host innate immune pathways in streptozotocin-induced diabetic hosts leads to more severe disease during infection with Burkholderia pseudomallei

2011-12-30 | GSE28683 | GEO

The Condition-Dependent Transcriptional Landscape of Burkholderia pseudomallei

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

The Condition-Dependent Transcriptional Landscape of Burkholderia pseudomallei

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

Comparative transcriptomics of Burkholderia pseudomallei from soil media and infected host

Project description:Burkholderia pseudomallei can adapt to and thrive in a variety of environments, including soil and water, and also can infect different hosts, including humans, leading to the tropical disease melioidosis. Modulation of gene and protein expression is one of this pathogen's adaptive survival mechanisms, which could lead to changes in the bacteria's cell membrane, metabolism, and virulence. To better understand bacterial adaptation and host-pathogen interactions, this study compared the expression profiles of B. pseudomallei from infected mice to B. pseudomallei cultivated in soil extract media. B. pseudomallei in vivo was created by infecting mice through the intraperitoneal route and harvesting the spleens on day 5 post infection. Total RNA was isolated and sequenced from the harvested spleen. Sequence reads were mapped to the B. pseudomallei UKMD286 strain genome sequence.

2022-07-22 | E-MTAB-11200 | biostudies-arrayexpress

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

2024-03-06 | GSE244127 | GEO

Delayed activation of host innate immune pathways in streptozotocin-induced diabetic hosts leads to more severe disease during infection with Burkholderia pseudomallei

Project description:The purpose of this study was to develop a comprehensive picture of the STZ-diabetic host transcriptional response during the acute stage of melioidosis and investigate the interplay between the diabetic host response and Burkholderia pseudomallei. To adress this, we compared the transcriptome of infected STZ-diabetic liver and spleen with uninfected STZ-diabetic tissues over an infection period of 42 hr (16 hpi, 24 hpi and 42 hpi, respectively) to identify genes whose expression is altered in response to an acute infection. The microarray experimental design included 3 biological replicates for each time point and both liver and spleen were harvested for RNA extraction. The microarray data from each time point was compared relative to uninfected diabetic mice. In addition, the transcriptome of uninfected STZ-diabetic liver and spleen were also compared with uninfected buffer (sodium citrate) control mice.

2011-12-30 | E-GEOD-28683 | biostudies-arrayexpress

Dual RNA-seq reveals a type 6 secretion system-dependent blockage of TNF-alpha signaling and BicA as a Burkholderia pseudomallei virulence factor important during gastrointestinal infection

Project description:Melioidosis is a disease caused by the Gram-negative bacillus Burkholderia pseudomallei (Bpm), commonly found in soil and water of endemic areas. Naturally acquired human melioidosis infections can result from either exposure through percutaneous inoculation, inhalation, or ingestion of soil-contaminated food or water. Our prior studies recognized Bpm as an effective enteric pathogen, capable of establishing acute or chronic gastrointestinal infections following oral inoculation (Sanchez-Villamil, Tapia et al. 2020). However, the specific mechanisms and virulence factors involved in the pathogenesis of Bpm during intestinal infection are unknown. In our current study, we standardized an in vitro intestinal infection model using mouse primary intestinal epithelial cells (mIECs) and demonstrated that Bpm requires a functional T6SS for full virulence. Further, we performed dual RNA-seq analysis on Bpm-infected mIECs to evaluate differentially expressed host and bacterial genes in the presence or absence of a T6SS. Our results showed a dysregulation in the TNF- signaling via NF-B pathway in the absence of the T6SS, with some of the genes involved in inflammatory processes and cell death also affected. Analysis of the bacterial transcriptome identified virulence factors and regulatory proteins playing a role during infection, with association to the T6SS. By using a Bpm transposon mutant library and isogenic mutants, we showed that deletion of the bicA gene, encoding a putative T3SS/T6SS regulator, ablated intracellular survival and plaque formation by Bpm and impacted survival and virulence when using murine models of acute and chronic gastrointestinal infection. Overall, these results highlight the importance of the type 6 secretion system in the gastrointestinal pathogenesis of Bpm.

2022-08-15 | GSE201263 | GEO

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