Bacillus anthracis str. Sterne
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ABSTRACT:
PROVIDER: PRJNA369565 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Investigation of whole genome expression level changes in Bacillus anthracis Sterne deltaClpX mutant compared to the wild-type strain after growth in nutrient rich media. The deltaClpX mutant used in this study is described in McGillivray et al. 2009. ClpX Protease Contributes to Antimicrobial Peptide Resistance and Virulence Phenotypes of Bacillus anthracis. Journal of Innate Immunity 1(5): 494-506.
2018-02-14 | GSE94398 | GEO
Project description:Bacillus anthracis str. Sterne Genome sequencing
| PRJNA236483 | ENA
Project description:Bacillus anthracis Sterne 34F2 cells were grown in the absence of and in the presence of different concentrations of paraquat and hydrogen peroxide. Additionally, a deletion mutant strain lacking the sodA1 gene was also assayed with and without the addition of different concentrations of paraquat.
2007-04-12 | E-MEXP-1043 | biostudies-arrayexpress
Project description:Bacillus anthracis strain:sterne strain Genome sequencing
| PRJNA545719 | ENA
Project description:Bacillus anthracis strain:delta Sterne Phenotype or Genotype
| PRJNA243519 | ENA
Project description:Bacillus anthracis strain:Sterne 09RA8929 Genome sequencing and assembly
| PRJNA422985 | ENA
Project description:Bacillus anthracis strain:Sterne 34F2 Genome sequencing and assembly
| PRJNA357857 | ENA
Project description:Effects of iron starvation on the transcriptional profile of Bacillus anthracis
2010-07-22 | E-MEXP-2272 | biostudies-arrayexpress
Project description:The lung is the entry site for Bacillus anthracis in inhalation anthrax, the most deadly form of the disease. Spores must escape through the alveolar epithelial cell (AEC) barrier and migrate to regional lymph nodes, germinate and enter the circulatory system to cause disease. Several mechanisms to explain alveolar escape have been postulated, and all these tacitly involve the AEC barrier. In this study, we incorporate our primary human type I AEC model, microarray gene profiling and gene enrichment analysis to study the response of AEC to B. anthracis, (Sterne) spores at 4 and 24 hours post-exposure. Spore exposure altered gene expression in AEC after 4 and 24 hours and differentially expressed genes (±1.3 fold, p ≤ 0.05) included CCL4/MIP-1β (4 hours), CXCL8/IL-8 (4 and 24 hours) and CXCL5/ENA-78 (24 hours). Gene enrichment analysis revealed that pathways involving cytokine or chemokine activity, receptor binding, and innate immune responses to infection were prominent. Microarray results were confirmed by qRT-PCR and multiplex ELISA assays. Chemotaxis assays demonstrated that spores induced the release of biologically active neutrophil and monocyte chemokines, and that CXCL8/IL-8 was the major neutrophil chemokine. The small or sub-chemotactic doses of CXCL5/ENA-78, CXCL3/GROββ and CCL20/MIP-3α may contribute to chemotaxis by priming effects. These data provide the first whole transcriptomic description of the human type I AEC initial response to B. anthracis spore exposure, and contribute to an increased understanding of the role of AEC in the pathogenesis of inhalational anthrax. We used microarrays to create a whole transcriptomic description of the response of primary human type I alveolar epithelial cells to B. anthracis spore exposure and demonstrated that several of the most upregulated differentially expressed genes included those for neutrophil and monocyte chemokines.
2018-08-03 | GSE102106 | GEO
Project description:The spore forming pathogen Bacillus anthracis is the etiologic agent of anthrax in humans and animals. It cycles through infected hosts as vegetative cells and is eventually introduced into the environment where it generates an endospore resistant to many harsh conditions. The endospores are subsequently ingested by the next host to begin the next cycle. Outbreaks of anthrax occur regularly worldwide in wildlife and livestock, and the potential for human infection exists whenever humans encounter infected animals. It is also possible to encounter intentional releases of anthrax spores, as was the case in October 2001. Consequently, it is important to be able to rapidly establish the provenance of infectious strains of B. anthracis. Here, we compare protein expression in seven low-passage wild isolates and four laboratory strains of B. anthracis grown under identical conditions using LC-MS/MS proteomic analysis. Of the 1,023 total identified proteins, 96 had significant abundance differences between wild and laboratory strains. Of those, 28 proteins directly related to sporulation were upregulated in wild isolates, with expression driven by Spo0A, CodY, and AbrB/ScoC. In addition, we observed evidence of changes in cell division and fatty acid biosynthesis between the two classes of strains, despite being grown under identical experimental conditions. These results suggest wild B. anthracis cells are more highly tuned to sporulate than their laboratory cousins, and this difference should be exploited as a method to differentiate between laboratory adapted cultures and low passage wild strains isolated during an anthrax outbreak. This knowledge should distinguish between intentional releases and exposure to strains in nature providing a basis for the type of response by public health officials and investigators.
2018-12-04 | PXD010120 | Pride