E-GEOD-70819
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA289649
PROVIDER: E-GEOD-70819 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-70819-analysis-methods.tsv | Tabular | |||
| E-GEOD-70819-analytics.tsv | Tabular | |||
| E-GEOD-70819-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-70819-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-70819-analytics.tsv.unrounded | Tabular |
Items per page: 5 1 - 5 of 34 |
Similar Datasets
Project description:Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague
| PRJNA289649 | ENA
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: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:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was “cell movement” including E-selectin, which was coordinately regulated with IL-1. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1, which together with IFN-, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease. 6 ENL skin lesions and 7 Lepromatous leprosy skin lesions
2009-06-30 | E-GEOD-16844 | biostudies-arrayexpress
Project description:Transcription profiling of mouse embryonic day 13.5 and 15.5 fetal livers lacking p38alpha, a mitogen-activated kinase that controls inflammatory responses and cell proliferation
2014-07-15 | E-GEOD-7342 | ExpressionAtlas
Project description:Neutrophils are innate immune cells involved in the elimination of pathogens. Recent studies showed that neutrophils can also act as antigen presenting cells (APC) to induce adaptive immune responses. Specific neutrophil populations (Na and Nb) with different levels of APC markers and in vitro distinct capacity to generate vaccinia virus (VACV)-specific CD8 T cell responses have been shown. However, how these neutrophil subtypes exert their role in vivo and how manipulation of Nb/Na ratio can influence vaccine-mediated immune responses are not known. In the context of VACV infection, we characterized HIV-specific CD8 T cell responses, delineated neutrophil transcriptomic profiles and described neutrophil dynamic behaviors in the spleen. By splenic multiphoton intravital microscopy (MV-IVM), we could distinguish both neutrophil subtypes and found that they showed distinct migratory and motility patterns and different ability to interact with CD8 T cells and move towards them. After analysis of adhesion, inflammatory and migration receptors from peritoneal cavity, blood and spleen, we defined that Nb neutrophils overexpressed the trans-endothelial migration marker a4b1integrin compared to Na subtype. Finally, by inhibiting a4b1integrin, we increased the Nb/Na ratio in peritoneal cavity and spleen, and in turn enhanced CD8 T cell responses to HIV-antigens. These findings provide significant advancements in the comprehension of neutrophil-based control of adaptive immune system. These results are relevant in vaccine vector design that could induce distinct neutrophil subtypes and, in consequence modulate antigen-specific T cell responses.
2021-04-12 | GSE165227 | GEO
Project description:Dunster2014 - WBC Interactions (Model1)
This is a sub-model of a three-step
inflammatory response modelling study. The model includes distinct
populations of white blood cells namely, macrophages and active and
apoptotic neutrophil populations. Neutrophil apoptosis rate is
predicted to be crucial for the qualitative nature of the
system.
This model is described in the article:
The resolution of
inflammation: a mathematical model of neutrophil and macrophage
interactions.
Dunster JL, Byrne HM, King JR.
Bull. Math. Biol. 2014 Aug; 76(8):
1953-1980
Abstract:
There is growing interest in inflammation due to its
involvement in many diverse medical conditions, including
Alzheimer's disease, cancer, arthritis and asthma. The
traditional view that resolution of inflammation is a passive
process is now being superceded by an alternative hypothesis
whereby its resolution is an active, anti-inflammatory process
that can be manipulated therapeutically. This shift in mindset
has stimulated a resurgence of interest in the biological
mechanisms by which inflammation resolves. The
anti-inflammatory processes central to the resolution of
inflammation revolve around macrophages and are closely related
to pro-inflammatory processes mediated by neutrophils and their
ability to damage healthy tissue. We develop a spatially
averaged model of inflammation centring on its resolution,
accounting for populations of neutrophils and macrophages and
incorporating both pro- and anti-inflammatory processes. Our
ordinary differential equation model exhibits two outcomes that
we relate to healthy and unhealthy states. We use bifurcation
analysis to investigate how variation in the system parameters
affects its outcome. We find that therapeutic manipulation of
the rate of macrophage phagocytosis can aid in resolving
inflammation but success is critically dependent on the rate of
neutrophil apoptosis. Indeed our model predicts that an
effective treatment protocol would take a dual approach,
targeting macrophage phagocytosis alongside neutrophil
apoptosis.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000616.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000616 | BioModels
Project description:Defects in neutrophil number and survival are common to both hematologic disorders and chronic inflammatory diseases. At sites of inflammation, neutrophils respond to multiple signals that activate protein kinase A (PKA) signalling, which positively regulates neutrophil survival. We aimed to study the transcriptional responses to several stimuli in human neutrophils. We used microarrays to detail the global programme of gene expression and identified distinct classes of up-regulated genes, which pointing to a key role of NR4A receptors in regulation of neutrophil lifespan and homeostasis.
2017-04-03 | GSE94923 | GEO
Project description:The circadian clock orchestrates vital physiological processes such as metabolism, immune function, and tissue regeneration, aligning them with the optimal time of day. This study identifies an intricate interplay between the circadian clock within muscle stem cells (SCs) and their capacity to modulate the immune microenvironment during muscle regeneration. We uncover that the SC clock provokes time-of-day (TOD)-dependent induction in inflammatory response genes following injury, particularly those related to neutrophil activity and chemotaxis. These responses are driven by rhythms of cytosolic regeneration of the signaling metabolite NAD+. We demonstrate that genetically enhancing cytosolic NAD+ regeneration in SCs is sufficient to induce robust inflammatory responses that significantly influence muscle regeneration. Furthermore, using mononuclear single-cell sequencing of the regenerating muscle niche, we uncover a key role for the cytokine CCL2 in mediating SC-neutrophil crosstalk in a TOD-dependent manner. Our findings highlight a crucial intersection between SC metabolic shifts and immune responses within the muscle microenvironment, dictated by the circadian rhythms, and underscore the potential for targeting circadian and metabolic pathways to enhance tissue regeneration.
2025-03-12 | GSE278177 | GEO
Project description:The circadian clock orchestrates vital physiological processes such as metabolism, immune function, and tissue regeneration, aligning them with the optimal time of day. This study identifies an intricate interplay between the circadian clock within muscle stem cells (SCs) and their capacity to modulate the immune microenvironment during muscle regeneration. We uncover that the SC clock provokes time-of-day (TOD)-dependent induction in inflammatory response genes following injury, particularly those related to neutrophil activity and chemotaxis. These responses are driven by rhythms of cytosolic regeneration of the signaling metabolite NAD+. We demonstrate that genetically enhancing cytosolic NAD+ regeneration in SCs is sufficient to induce robust inflammatory responses that significantly influence muscle regeneration. Furthermore, using mononuclear single-cell sequencing of the regenerating muscle niche, we uncover a key role for the cytokine CCL2 in mediating SC-neutrophil crosstalk in a TOD-dependent manner. Our findings highlight a crucial intersection between SC metabolic shifts and immune responses within the muscle microenvironment, dictated by the circadian rhythms, and underscore the potential for targeting circadian and metabolic pathways to enhance tissue regeneration.
2025-03-12 | GSE278176 | GEO