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ABSTRACT: Analysis of 3800-year-old Yersinia pestis genomes suggests Bronze Age origin for bubonic plague

PROVIDER: PRJEB24296 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2261880.fastq.gz	Fastqsanger.gz
	ERR2261881.fastq.gz	Fastqsanger.gz
	ERR2261882.fastq.gz	Fastqsanger.gz
	ERR2261883.fastq.gz	Fastqsanger.gz
	ERR2261884.fastq.gz	Fastqsanger.gz

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Stone Age Yersinia pestis genomes shed light on the early evolution, diversity and ecology of plague

Project description:Late Neolithic/Early Bronze Age Yersinia pestis genomes

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CRISPR-Cas9 mutagenesis of U937 cells for variants resistant to Yersinia pestis intoxication

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Ancient Yersinia pestis and Salmonella enterica genomes from Bronze Age Crete

Project description:Ancient Yersinia pestis and Salmonella enterica genomes from Bronze Age Crete

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Role of the Yersinia pestis Virulence Plasmid in Evading a Protective Polymorphonuclear Leukocyte Response During the Early Stages of Bubonic Plague

Project description:A delay in the mammalian inflammatory response is a prominent feature of infection with Yersinia pestis, the agent of bubonic and pneumonic plague. Y. pestis factors have been identified that either do not stimulate a normal inflammatory response, or actively suppress it. Prominent among these are components of the Type III secretion system that is encoded on the Yersinia virulence plasmid (pYV). We used a rat model of bubonic plague to characterize the kinetics and extent of the mammalian transcriptomic response to infection with wild-type or pYV-negative Y. pestis in the draining lymph node. Remarkably, dissemination and multiplication of wild-type Y. pestis during the bubonic stage of disease did not induce any detectable gene expression response by host lymph node cells. This was followed, however, by an extensive transcriptomic response, including upregulation of several cytokine, chemokine, and other immune response genes, after systemic spread during septicemic plague. Matched lymph node samples used for histopathology and extracellular cytokine measurements, combined with the microarray data set, broadly outlined the mammalian immune response to Y. pestis and how it is influenced by pYV-encoded factors. The results indicate that both WT and pYV– Y. pestis induce primarily a Th17 response, and not a Th1 or Th2 response. In the absence of pYV, a sustained recruitment of polymorphonuclear leukocytes, the major Th17 effector cell, to the lymph node resulted in clearance of infection. Thus, the ability to counteract a Th17- driven PMN response in the lymph node appears to be a major function of the Y. pestis virulence plasmid. In contrast, classic markers of the proinflammatory response and macrophage activation, such as TNF-á and IFN-ã, were not induced at all by pYV– Y. pestis, and appeared only late in infection with WT Y. pestis. Rats treated with PBS and Yersinia pestis at various time points.

2010-12-07 | E-GEOD-22299 | biostudies-arrayexpress

Global gene expression analysis of Yersinia pestis Ype AHL quorum sensing at 30°C

Project description:Quorum sensing is a cell to cell communication process that involves chemical signaling. Yersinia pestis, the agent of plague, has two functional AHL quorum sensing systems Ysp and Ype. For several reasons, it was not clear what effect AHL pathways have on virulence gene expression and survival in the two different hosts, flea and human. To investigate to what effect AHL quorum sensing has on gene expression, we conducted microarray studies comparing Yersinia pestis CO92 (∆pgm) to a double AHL mutant strain (∆pgm ΔypeIR) at 30°C.

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Global gene expression analysis of Yersinia pestis AHL quorum sensing at 37°C

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Global gene expression analysis of Yersinia pestis Ysp AHL quorum sensing at 30°C

Project description:Quorum sensing is a cell to cell communication process that involves chemical signaling. Yersinia pestis, the agent of plague, has two functional AHL quorum sensing systems Ysp and Ype. For several reasons, it was not clear what effect AHL pathways have on virulence gene expression and survival in the two different hosts, flea and human. To investigate to what effect Ysp AHL quorum sensing has on gene expression, we conducted microarray studies comparing Yersinia pestis CO92 (∆pgm) to a single AHL mutant strain (∆pgm ΔyspI) at 30°C.

2016-01-01 | GSE30329 | GEO

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2016-01-01 | GSE30341 | GEO

Primary pneumonic vs cultured Y. pestis

Project description:Although pneumonic plague is the deadliest manifestation of disease caused by the bacterium Yersinia pestis, there is surprisingly little information on the cellular and molecular mechanisms responsible for Y. pestis-triggered pathology in the lung. Therefore, to understand the progression of this unique disease, we developed an intranasal mouse model of primary pneumonic plague. Mice succumbed to a purulent multifocal severe exudative bronchopneumonia that closely resembles the disease observed in humans. In order to assess the adaptation of Y. pestis to a mammalian environment, we employed DNA microarray technology to analyze the transcriptional responses of the bacteria during interaction with the mouse lung as compared to bacteria cultured in vitro. Keywords: Infectious expression analysis

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