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Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE70819 | GEO | 2015/07/13

SECONDARY ACCESSION(S): PRJNA289649

REPOSITORIES: GEO

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Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague

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.

2015-07-13 | E-GEOD-70819 | biostudies-arrayexpress

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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

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Project description:Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague

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Project description:Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague

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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

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2010-12-07 | GSE22299 | GEO

RNA-seq analysis of pathogen and host in the early stages of Plague pulmonary infection using a novel dual RNA extraction method

Project description:The goal of this study is to determine the host and pathogen transcriptomic response during pneumonic plague infection. Mice were infected intranasally with high dose of 800,000 cfu/mouse (1500 LD50). Mice were sacrificed at 1, 24 and 48 hours post infection and dual RNA was extracted. In order to isolate high quantities of superior quality mRNA from bacteria and mice we used a novel technique, that employed infusion of an RNA preserving reagent (RNAlater) into the lungs of the animals through the trachea under deep anesthesia prior to the collection of the organs. Unprecedently, this method enables isolation of stable dual mRNA from lungs of mice infected with Y. pestis, as early as 24 hours post infection. RNA-seq libraries were generated and sequencing of 100bp paired-end was performed on the Illumina NovaSeq 6000 system. The RNA was used for transcriptomic analyses which provided a comprehensive gene-expression profile of both the host and pathogen at 24 and 48 hours post infection.

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