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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE133826 | GEO | 2019/07/04

REPOSITORIES: GEO

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Transcriptional analysis of ypeIR mutation in Yersinia pestis at 37°C

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

Comparison of Yersinia pestis from rat buboes and laboratory cultures

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

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 AHL quorum sensing at 37°C

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2016-01-01 | GSE30331 | GEO

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

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

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2016-01-01 | GSE30329 | GEO

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

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2016-01-01 | GSE30328 | GEO

Transcriptional analysis of AI-2 treatment in Yersinia pestis at 30°C

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

Transcriptional analysis of quorum sensing deficient in Yersinia pestis CO92 at 37°C

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2013-09-05 | GSE21911 | GEO

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

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