Bronze Age Plague
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB10885 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1018890.fastq.gz | Fastqsanger.gz | |||
| ERR1018900.fastq.gz | Fastqsanger.gz | |||
| ERR1018910.fastq.gz | Fastqsanger.gz | |||
| ERR1018920.fastq.gz | Fastqsanger.gz | |||
| ERR1018930.fastq.gz | Fastqsanger.gz |
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Project description:Yersinia pestis genomes reveal plague in Britain 4,000 years ago
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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
Project description:During pneumonic plague, the bacterium Yersinia pestis elicits the development of inflammatory lung lesions that continue to expand throughout infection. This lesion development and persistence is poorly understood. Here, we examine spatially distinct regions of lung lesions using laser capture microdissection and RNAseq analysis to identify transcriptional differences between lesion microenvironments. We show that cellular pathways involved in leukocyte migration and apoptosis are down regulated in the center of lung lesions compared to the periphery. Probing for the bacterial factor(s) important for the alteration in neutrophil survival, we show both in vitro and in vivo that Y. pestis increases neutrophil survival in a manner that is dependent on the type-III secretion system effector YopM. This research explores the complexity of spatially distinct host - microbe interactions and emphasizes the importance of cell relevance in assays in order to fully understand Y. pestis virulence.
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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.
2010-12-07 | GSE22299 | GEO
Project description:The Stone Age Plague: 1000 years of Persistence in Eurasia
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Project description:During pneumonic plague, the bacterium Yersinia pestis elicits the development of inflammatory lung lesions that continue to expand throughout infection. This lesion development and persistence is poorly understood. Here, we examine spatially distinct regions of lung lesions using laser capture microdissection and RNAseq analysis to identify transcriptional differences between lesion microenvironments. We show that cellular pathways involved in leukocyte migration and apoptosis are down regulated in the center of lung lesions compared to the periphery. Probing for the bacterial factor(s) important for the alteration in neutrophil survival, we show both in vitro and in vivo that Y. pestis increases neutrophil survival in a manner that is dependent on the type-III secretion system effector YopM. This research explores the complexity of spatially distinct host - microbe interactions and emphasizes the importance of cell relevance in assays in order to fully understand Y. pestis virulence. We examine spatially distinct regions of lung lesions using laser capture microdissection and RNAseq analysis to identify transcriptional differences between lesion microenvironments. Sample types: uninfected BM-PMN, infected BM-PMN, lesion periphery, lesion center.
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Project description:Yersinia pestis, the etiologic agent of plague, emerged as a flea-borne pathogen only within the last 6,000 years. Just five simple genetic changes in the Yersinia pseudotuberculosis progenitor, which served to eliminate toxicity to fleas and to enhance survival and biofilm formation in the flea digestive tract, were key to the transition to the arthropod-borne transmission route. To gain a deeper understanding of the genetic basis for the development of a transmissible biofilm infection in the flea foregut, we evaluated additional gene differences and performed in vivo transcriptional profiling of Y. pestis, Y. pseudotuberculosis wild-type (unable to form biofilm in the flea foregut), and a Y. pseudotuberculosis mutant strain (able to produce foregut-blocking biofilm in fleas) recovered from fleas 1 day and 14 days after an infectious bloodmeal. Surprisingly, the Y. pseudotuberculosis mutations that increased c-di-GMP levels and enabled biofilm development in the flea did not change expression levels of the hms genes responsible for the synthesis and export of the extracellular polysaccharide matrix required for mature biofilm formation. The Y. pseudotuberculosis mutant uniquely expressed much higher levels of one of the Yersinia Type VI secretion systems (T6SS-4) in the flea, and this locus was required for flea blockage by Y. pseudotuberculosis, but not by Y. pestis. Significant differences between the two species in expression of several metabolism genes, the Psa fimbrial genes, quorum sensing related genes, transcriptional regulators, and stress response genes were evident during flea infection. The results provide insights into how Y. pestis has adapted to life in its flea vector and point to evolutionary changes in the regulation of biofilm development pathways in these two closely related species
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Project description:The rapid pace of bacterial evolution enables organisms to adapt to the laboratory environment with repeated passage and thus diverge from naturally-occurring environmental (“wild”) strains. Distinguishing wild and laboratory strains is clearly important for biodefense and bioforensics; however, DNA sequence data alone has thus far not provided a clear signature, perhaps due to lack of understanding of how diverse genome changes lead to convergent phenotypes, difficulty in detecting certain types of mutations, or perhaps because some adaptive modifications are epigenetic. Monitoring protein abundance, a molecular measure of phenotype, can overcome some of these difficulties. We have assembled a collection of Yersinia pestis proteomics datasets from our own published and unpublished work, and from a proteomics data archive, and demonstrated that protein abundance data can clearly distinguish laboratory-adapted from wild. We developed a lasso logistic regression classifier that uses binary (presence/absence) or quantitative protein abundance measures to predict whether a sample is laboratory-adapted or wild that proved to be ~98% accurate, as judged by replicated 10-fold cross-validation. Protein features selected by the classifier accord well with our previous study of laboratory adaptation in Y. pestis. The input data was derived from a variety of unrelated experiments and contained significant confounding variables. We show that the classifier is robust with respect to these variables. The methodology is able to discover signatures for laboratory facility and culture medium that are largely independent of the signature of laboratory adaptation. Going beyond our previous laboratory evolution study, this work suggests that proteomic differences between laboratory-adapted and wild Y. pestis are general, potentially pointing to a process that could apply to other species as well. Additionally, we show that proteomics datasets (even archived data collected for different purposes) contain the information necessary to distinguish wild and laboratory samples. This work has clear applications in biomarker detection as well as biodefense.
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Project description:Microarrays were used to determine the transcriptional profile of Y. pestis that is growing inside macrophages. J774A.1 macrophage-like cells were infected with Y. pestis KIM5 and incubated in the presence of gentamicin in tissue culture media. RNA was isolated from intracellular bacteria at various time points post infection. Control bacteria were grown for 4 hours in tissue culture medium under the same conditions without macrophages or gentamicin. The transcriptional profiles of intracellular Y. pestis at different time points were compared to those of control Y. pestis using the 70-mer oligonucleotide microarrays obtained from Pathogen Functional Genomics Resource Center/J. Craig Venter Institute (Y. pestis microarray version 2). RNA from samples of Yersinia pestis KIM5 at 3 time points in were compared to 12 Yersinia pestis in DMEM for 4 hours.
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