Molecular alterations induced by Yersinia pestis, dengue virus and Staphylococcus enterotoxin B under the background of battlefield-like stress (microarray)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA479982 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide alterations of gene expression were characterized using leukocytes collected from (informed and consented, all male) U.S. Army Ranger cadets immediately before and after training followed by exposure to a representative group of pathogens Yersinia pestis, dengue virus, Staphylococcus enterotoxin B. We employed experimental and computational approaches in identifying altered molecules, processes, pathways, and functional and regulatory networks mediating the host’s response towards battlefield-like stress, in assessing protective immunity status of the stressed host towards infection, and in identifying pathogen-induced biomarkers under severe stress background. We observed predicted inhibition of pathways significantly associated with lymphopoiesis, wound healing, inflammatory response, lymphocyte activation, apoptosis, and predicted activation of oxidative stress. Using weighted correlation network analyses, we showed preservation of these pathways across infection plus stress combinations. Regulatory networks comprising a common set of upstream regulators: transcription factors, microRNAs and post-translational regulators (kinases, phosphatases) may be drivers of molecular alterations leading compromised protective immunity. Other sets of transcripts were persistently altered in both the pre- and post-stress conditions due to the host’s response to each pathogen forming pathogen-specific molecular signatures with a potential to distinguish infection from that of severe stress. Our results suggest that severe battlefield-like stress alters molecular players implicated in the developments of hematopoietic stem cells probably leading to depletion of cellular and molecular repertoires of protective immunity, membrane trafficking of recycling endosomes and membrane translocation of the antigen processing mechanisms leading to suboptimal antigen processing and presentation, cell adhesion leading to impaired formation of productive immunological synapse, and inhibited T-cell activation. These factors may collectively be responsible for compromised protective immunity (infection susceptibility, delayed wound healing and poor vaccine response), and cellular anergy.
2021-07-05 | GSE116725 | GEO
Project description:Background: Severe stress can have drastic and systemic effects with dire implications on the health and wellbeing of exposed individuals. Particularly, the effect of stress on the immune response to infection is of interest because of its implications for vaccine efficacy and treatment strategy during stressful scenarios. Battlefield-like stress has previously been shown to cause an anergic state in the immune system that persists following exposure to a potent mitogen. Methods: Genome-wide alterations of gene expression were characterized using leukocytes collected from (15 informed and consented, all male) U.S. Army Ranger cadets immediately before and after training followed by exposure to a representative group of pathogens Yersinia pestis, dengue virus, Staphylococcus enterotoxin B (SEB). We employed experimental and computational approaches in identifying altered molecules, processes, pathways, and functional and regulatory networks mediating the host’s response towards battlefield-like stress, in assessing protective immunity status of the stressed host towards infection, and in identifying pathogen-induced biomarkers under severe stress background. Results: We observed predicted inhibition of pathways significantly associated with lymphopoiesis, wound healing, inflammatory response, lymphocyte activation, apoptosis, and predicted activation of oxidative stress. Using weighted correlation network analyses, we showed preservation of these pathways across infection plus stress combinations. Regulatory networks comprising a common set of upstream regulators: transcription factors, microRNAs and post-translational regulators (kinases, phosphatases) may be drivers of molecular alterations leading compromised protective immunity. Other sets of transcripts were persistently altered in both the pre- and post-stress conditions due to the host’s response to each pathogen forming pathogen-specific molecular signatures with a potential to distinguish infection from that of severe stress. Conclusion: Our results suggest that severe battlefield-like stress alters molecular players implicated in the developments of hematopoietic stem cells probably leading to depletion of cellular and molecular repertoires of protective immunity, membrane trafficking of recycling endosomes and membrane translocation of the antigen processing mechanisms leading to suboptimal antigen processing and presentation, cell adhesion leading to impaired formation of productive immunological synapse, and inhibited T-cell activation. These factors may collectively be responsible for compromised protective immunity (infection susceptibility, delayed wound healing and poor vaccine response), and cellular anergy.
2021-07-05 | GSE117464 | GEO
Project description:Molecular alterations induced by Yersinia pestis, dengue virus and Staphylococcus enterotoxin B under the background of battlefield-like stress
| PRJNA482156 | ENA
Project description:Molecular alterations induced by Yersinia pestis, dengue virus and Staphylococcus enterotoxin B under the background of battlefield-like stress (miRNA-Seq)
| PRJNA482157 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-07-05 | GSE117465 | GEO
Project description:Transcriptome alterations of leukocytes from soldiers who underwent eight-weeks of Army Ranger training (RASP, Ranger Assessment and Selection Program) were analyzed to evaluate impacts of battlefield-like stress on the immune response. About 1,400 transcripts were differentially expressed between pre- and post-RASP leukocytes. Upon functional analysis, immune response was the most enriched biological process, and most of the transcripts associated with the immune response were down-regulated. Microbial pattern recognition, chemotaxis, antigen presentation, and T-cell activation were among the most down-regulated immune processes. Post-RASP leukocytes exposed ex vivo to Staphylococcal enterotoxin B (SEB) showed a markedly impaired immune response to this superantigen compared to pre-RASP leukocytes, consistent with suppression of the immune response revealed by transcriptome analyses.
2014-10-27 | GSE39148 | GEO
Project description:Whole blood RNA (PAXgene tubes) was collected from 14 Dengue patients after hospital admission. Additional samples were collected at later time points from 6 of the patients, and single samples were also collected from 4 healthy donors. RNA was amplified using the MessageAmp kit (Ambion), and reverse transcribed. Each sample was labelled with Cy5, and hybridized to a Lymphochip cDNA array along with amplified human reference RNA labelled with Cy3(Universal Human Reference RNA, Stratagene). Analysis was restricted to those array elements (LUIDs) with signal intensity/background of at least 2.5 in either channel for at least 80% (28/34) of the samples, and a regression correlation of 0.6. We characterized gene expression patterns associated with acute dengue infection, and identified a set of transcripts associated with diagnosis of Dengue Shock Syndrome. disease_state_design
2012-09-06 | E-GEOD-40628 | biostudies-arrayexpress
Project description:Whole blood RNA (PAXgene tubes) was collected from 14 Dengue patients after hospital admission. Additional samples were collected at later time points from 6 of the patients, and single samples were also collected from 4 healthy donors. RNA was amplified using the MessageAmp kit (Ambion), and reverse transcribed. Each sample was labelled with Cy5, and hybridized to a Lymphochip cDNA array along with amplified human reference RNA labelled with Cy3(Universal Human Reference RNA, Stratagene). Analysis was restricted to those array elements (LUIDs) with signal intensity/background of at least 2.5 in either channel for at least 80% (28/34) of the samples, and a regression correlation of 0.6. We characterized gene expression patterns associated with acute dengue infection, and identified a set of transcripts associated with diagnosis of Dengue Shock Syndrome.
2012-09-06 | GSE40628 | GEO
Project description:Background The osmotic regulator OmpR in Escherichia coli regulates differentially the expression of major porin proteins OmpF and OmpC. In Yersinia enterocolitica and Y. pseudotuberculosis, OmpR is required for both virulence and survival within macrophages. However, the phenotypic and regulatory roles of OmpR in Y. pestis are not yet fully understood. Results Y. pestis OmpR is involved in building resistance against phagocytosis and controls the adaptation to various stressful conditions met in macrophages. The ompR mutation likely did not affect the virulence of Y. pestis strain 201 that was a human-avirulent enzootic strain. The microarray-based comparative transcriptome analysis disclosed a set of 224 genes whose expressions were affected by the ompR mutation, indicating the global regulatory role of OmpR in Y. pestis. Real-time RT-PCR or lacZ fusion reporter assay further validated 16 OmpR-dependent genes, for which OmpR consensus-like sequences were found within their upstream DNA regions. ompC, F, X, and R were up-regulated dramatically with the increase of medium osmolarity, which was mediated by OmpR occupying the target promoter regions in a tandem manner. Conclusion OmpR contributes to the resistance against phagocytosis or survival within macrophages, which is conserved in the pathogenic yersiniae. Y. pestis OmpR regulates ompC, F, X, and R directly through OmpR-promoter DNA association. There is an inducible expressions of the pore-forming proteins OmpF, C, and X at high osmolarity in Y. pestis, in contrast to the reciprocal regulation of them in E. coli. The main difference is that ompF expression is not repressed at high osmolarity in Y. pestis, which is likely due to the absence of a promoter-distal OmpR-binding site for ompF.
2011-10-24 | GSE26601 | GEO
Project description:These 40 microarray datasets represent whole blood samples from 31 primary dengue infection patients and 9 healthy volunteers from Managua, Nicaragua. The dengue infection patients include both primary dengue fever (DF) and primary dengue hemorrhagic fever (DHF) cases.
2018-07-31 | GSE96656 | GEO