Chlorocebus aethiops
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PROVIDER: PRJNA268214 | ENA |
REPOSITORIES: ENA
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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: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:Pneumonic plague is the most deadly form of infection caused by Yersinia pestis and can progress extremely fast. However, our understanding on the host transcriptomic response to pneumonic plague is insufficient. Here, we used RNA-sequencing technology to analyze transcriptomic responses in mice infected with fully virulent strain 201 or EV76, a live attenuated vaccine strain lacking the pigmentation locus. Approximately 600 differentially expressed genes (DEGs) were detected in lungs from both 201- and EV76-infected mice at 12 hours post-infection (hpi). DEGs in lungs of 201-infected mice exceeded 2,000 at 48 hpi, accompanied by sustained large numbers of DEGs in the liver and spleen; however, limited DEGs were detected in those organs of EV-infected mice. Remarkably, DEGs in lungs were significantly enriched in critical immune responses pathways in EV76-infected but not 201-infected mice, including antigen processing and presentation, T cell receptor signaling among others. Pathological and bacterial load analyses confirmed the rapid systemic dissemination of 201-infection and the confined EV76-infection in lungs. Our results demonstrate that fully virulent Y. pestis strongly inhibits both the innate and adaptive immune responses that are substantially stimulated in a self-limited infection, which update our holistic views on the transcriptomic response to pneumonic plague.
2017-07-13 | GSE84341 | 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: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.
2015-07-13 | GSE70819 | GEO
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
Project description:Initiation of treatment during the pre-symptomatic phase of infection with Yersinia pestis (Y. pestis) is particularly critical because the rapid proliferation of Y. pestis is coupled with the manifestation of common flu-like early symptoms that often delay the intervention. Our study used African Green Monkeys that didn’t exhibited clear clinical symptoms for nearly two days after intranasal challenge with Y. pestis and succumbed within a day after showing the first signs of clinical discomfort. Colonization of Y. pestis was detected in blood one day post-infection although blood transcripts were found to be altered immediately after the pathogenic assault. The organs of the respiratory tract and those adjacent, such as lungs and submandibular lymph nodes, accumulated significant Y. pestis colonization immediately after pathogenic challenge. Hence organ-specific molecular investigations are deemed to be the key in elucidation of the mechanisms of the initial host response. Based on results from our previous investigation of the blood transcriptomic profile, we explored the early involvement of the ubiquitin-microtubule-mediated host defense mechanism in detail. Genes enriching the ubiquitin network were altered, indicating an early suppression of the network functions in the submandibular lymph nodes. In concert, the upstream toll-like receptor signaling and downstream IκB kinase/NFκB signaling were inhibited at the transcription level. The inflammatory response was suppressed in the lungs, submandibular lymph nodes and mediastinal lymph nodes. By dysregulating both ubiquitin and the microtubule networks, Yersinia pestis was able to impair host-mediated proteolysis activities and evade autophagosome capture. A synchronized suppression of the immune response may render the peripheral organs more vulnerable to the imminent pathogenic assault. Furthermore, a comprehensive early onset of apoptosis was found across these three organ types. This was possibly a parallel mechanism undertaken by Yersinia pestis to further weaken the host response and enable a permissive colonization of the host. Targeting these networks in an organ-specific and time-resolved fashion could be essential for development of the next generation therapeutics for pneumonic plague.
2017-10-31 | GSE101653 | 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:Characterization of transcriptomic variation is emerging as a critical tool for understanding how quantitative trait loci (QTL) contribute to complex phenotypes. Human transcriptomic studies are limited by factors such as the feasibility of invasive tissue collection or variable environmental exposures that can be readily overcome in non-human primate (NHP) models. We characterized transcriptomic variation across multiple tissues and developmental stages and between individuals in 59 vervet monkeys from the Vervet Research Colony extended pedigree. We conducted RNA sequencing across early (7, 90 days, and one year) and later (1.25, 1.5, 1.75, 2, 2.5, 3, and 4+ years old) developmental time points in 6 individuals at each stage in five tissue types: two brain tissues from hippocampus and caudate, two endocrine tissues (pituitary and adrenal) and two peripheral tissues serving as a source of biomarkers (blood and fibroblasts)
2014-02-12 | E-MTAB-4404 | biostudies-arrayexpress
Project description:Patterns of microRNA Expression in Non-Human Primate
| PRJNA127979 | ENA