Evolution of Yersinia pestis in Eastern Europe
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB35426 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4626670_1.fastq.gz | Fastqsanger.gz | |||
| ERR4626670_2.fastq.gz | Fastqsanger.gz | |||
| ERR4624261_1.fastq.gz | Fastqsanger.gz | |||
| ERR4624261_2.fastq.gz | Fastqsanger.gz | |||
| ERR4624301_1.fastq.gz | Fastqsanger.gz |
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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
2005-11-10 | GSE3575 | GEO
Project description:The plague agent, Yersinia pestis, employs a type III secretion system (T3SS) to selectively destroy human immune cells, thereby enabling its replication in the bloodstream and transmission to new hosts via fleabite. The host factors responsible for the selective destruction of immune cells by plague bacteria were not known. Here we show that LcrV, the needle cap protein of the Y. pestis T3SS, binds N-formylpeptide receptor (FPR1) on human immune cells to promote the translocation of bacterial effectors.
2019-07-04 | GSE133826 | GEO
Project description:The etiologic agent of bubonic plague, Yersinia pestis, senses cell density-dependent chemical signals to synchronize transcription between cells of the population in a process named quorum sensing. Though the closely related enteric pathogen Y. pseudotuberculosis uses quorum sensing system to regulate motility, the role of YpeIR quorum sensing in Y. pestis has been unclear. YpeIR is one of the AHL quorum sensing system in Y. pestis. In this study we performed transcriptional profiling experiments to identify Y. pestis YpeIR quorum sensing regulated functions at 37°C.
2016-01-01 | GSE30341 | GEO
Project description:Yunnan Province, China is thought to be the original source of biovar Orientalis of Yersinia pestis, the causative agent of the third plague pandemic that has spread globally since the end of the 19th century. Although encompassing a large area of natural plague foci, Y. pestis strains have rarely been found in live rodents during surveillance in Yunnan, and most isolates are from rodent corpses and their fleas. In 2017, 10 Y. pestis strains were isolated from seven live rodents and three fleas in Heqing County (HQ) of Yunnan. These strains were supposed to have low virulence to local rodents Eothenomys miletus and Apodemus chevrieri because the rodents were healthy and no dead animals were found in surrounding areas, as had occurred in previous epizootic disease. We performed microscopic and biochemical examinations of the isolates,and compared their whole-genome sequences and transcriptome with those of 10 high virulence Y. pestis strains that were isolated from the adjacent city (Lijiang). We analyzed the phenotypic, genomic, and transcriptomic characteristics of live rodent isolates. The isolates formed a previously undefined monophyletic branch of Y. pestis that was named 1.IN5. Six SNPs, two indels, and one copy number variation were detected between live rodent isolates and the high virulence neighbors. No obvious functional consequence of these variations was found according to the known annotation information. Among the genes that were differentially expressed between the live rodent isolates and their high virulence neighbors, we detected five iron transfer-related genes that were significantly up-regulated in live rodent isolates compared with high virulence isolates (|log2 (FC) | >1, p.adjust <0.05), indicating these genes may be related to the low-virulence phenotype. The novel genotype of Y. pestis reported here provides further insights into the evolution and spread of plague as well as clues that may help to decipher the virulence mechanism of this notorious pathogen.
2021-04-20 | GSE161888 | GEO
Project description:Yersinia pestis causes bubonic plague in humans and rats. The disease is characterized by an enlarged, painful lymph node, termed a bubo, that develops following bacterial dissemination from an intradermal flea bite injection site. In susceptible animals, the bacteria quickly overcome host innate immune defenses in the lymph node, spread systemically through the blood, and produce fatal sepsis 1,2. At the terminal stage of disease, the bubo contains massive numbers of extracellular bacteria, necrotic lymphoid tissue, hemorrhage, and fibrin 2. The extreme virulence of Y. pestis has been largely ascribed to its ability to avoid innate immunity by preventing phagocytosis, selectively killing immune cells, and down regulating the proinflammatory response 3. Here we report that two innate immune effector mechanisms are generated during bubonic plague in the rat: iron limitation and nitrosative stress. The expression of nitric oxide synthase (iNOS) by rat polymorphonuclear neutrophils (PMNs) was induced in the bubo, and mutation of the Y. pestis hmp gene, which encodes a flavohemoglobin important for resistance to nitric oxide (NO), attenuated virulence. Thus, although Y. pestis avoids uptake and intracellular killing by phagocytes, it still encounters innate immune effector molecules, particularly phagocyte-derived reactive nitrogen species, in the extracellular environment of the bubo. Keywords: repeat
2006-07-28 | GSE3793 | GEO
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:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of autoinducer-2 (AI-2) quorum sensing was investigated by comparing transcript profiles when AI-2 quorum-sensing signal is added in to control. The strain Δpgm (pigmentation-negative) mutant was used as wild type.The control consisted of cells grown and treated under the same conditions without added signals.
2016-01-01 | GSE30237 | GEO
Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of quorum sensing was investigated by comparing transcript profiles when three quorum-sensing synthase genes are knocked out. Two strains, ∆pgm (pigmentation-negative) mutant R88 as treatment and quorum sensing null strain R115 with mutations (∆pgm, ∆ypeIR, ∆yspIR, and ∆luxS) as control, are used in this analysis.
2013-09-05 | GSE21911 | GEO
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:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of autoinducer 2 (AI-2) quorum sensing was investigated by comparing transcript profiles when luxS gene was knocked out. The luxS gene encodes S-ribosylhomocysteinase which can produce DPD, a precursor of AI-2. The strain ∆pgm (pigmentation-negative) mutant R88 was called wild type. The ∆pgm ∆luxS mutant was called control.
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