E-ENAD-41
Ontology highlight
ABSTRACT:
PROVIDER: E-ENAD-41 | ExpressionAtlas | 2020-04-22
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-ENAD-41-analysis-methods.tsv | Tabular | |||
| E-ENAD-41-atlasExperimentSummary.Rdata | Rdata | |||
| E-ENAD-41-coexpressions.tsv.gz | Tabular | |||
| E-ENAD-41-configuration.xml | Xml | |||
| E-ENAD-41-factors.xml | Xml |
Items per page: 5 1 - 5 of 281 |
Similar Datasets
Project description:Numerous bacterial pathogens utilize type 3 secretion systems that inject effector proteins into host immune cells to support their pathogenesis. We investigated the T3SS effectors (Yops) of Yersinia enterocolitica for their individual and combined effects on gene expression, inflammasome formation and Ca2+ signaling in primary human macrophages. The up- or down-regulation of thousands of macrophage genes by Yersinia inflammatory stimuli was effectively suppressed by YopP, which correlated with regulation of histone phosphorylation at H3S10ph, and YopM and YopQ systematically counteracting selected YopP transcriptional effects. Inflammasome formation was reduced by a combination of YopP and YopQ, but not by single effectors or other combinations of them. Intracellular Ca2+ transients were blocked by YopH alone. Thus, the T3SS effectors of Yersinia individually, synergistically or antagonistically suppress the major immune pathways of human macrophages to dampen the immune response.
2025-04-21 | E-MTAB-14995 | biostudies-arrayexpress
Project description:<p>The reverse transsulfuration pathway is the major route for the metabolism of sulfur-containing amino acids. The role of this metabolic pathway in macrophage response and function is unknown. We show that the enzyme cystathionine ?-lyase (CTH) is induced in macrophages infected with pathogenic bacteria through signaling involving phosphatidylinositol 3-kinase (PI3K)/MTOR and the transcription factor SP1. This results in the synthesis of cystathionine, which facilitates the survival of pathogens within myeloid cells. Our data demonstrate that the expression of CTH leads to defective macrophage activation by (i) dysregulation of polyamine metabolism by depletion of S-adenosylmethionine, resulting in immunosuppressive putrescine accumulation and inhibition of spermidine and spermine synthesis, and (ii) increased histone H3K9, H3K27, and H3K36 di/trimethylation, which is associated with gene expression silencing. Thus, CTH is a pivotal enzyme of the innate immune response that disrupts host defense. The induction of the reverse transsulfuration pathway by bacterial pathogens can be considered an unrecognized mechanism for immune escape.</p><p><strong>IMPORTANCE:</strong> Macrophages are professional immune cells that ingest and kill microbes. In this study, we show that different pathogenic bacteria induce the expression of cystathionine ?-lyase (CTH) in macrophages. This enzyme is involved in a metabolic pathway called the reverse transsulfuration pathway, which leads to the production of numerous metabolites, including cystathionine. Phagocytized bacteria use cystathionine to better survive in macrophages. In addition, the induction of CTH results in dysregulation of the metabolism of polyamines, which in turn dampens the proinflammatory response of macrophages. In conclusion, pathogenic bacteria can evade the host immune response by inducing CTH in macrophages.</p>
2020-07-29 | MSV000085845 | GNPS
Project description:<p>The reverse transsulfuration pathway is the major route for the metabolism of sulfur-containing amino acids. The role of this metabolic pathway in macrophage response and function is unknown. We show that the enzyme cystathionine γ-lyase (CTH) is induced in macrophages infected with pathogenic bacteria through signaling involving phosphatidylinositol 3-kinase (PI3K)/MTOR and the transcription factor SP1. This results in the synthesis of cystathionine, which facilitates the survival of pathogens within myeloid cells. Our data demonstrate that the expression of CTH leads to defective macrophage activation by (i) dysregulation of polyamine metabolism by depletion of S-adenosylmethionine, resulting in immunosuppressive putrescine accumulation and inhibition of spermidine and spermine synthesis, and (ii) increased histone H3K9, H3K27, and H3K36 di/trimethylation, which is associated with gene expression silencing. Thus, CTH is a pivotal enzyme of the innate immune response that disrupts host defense. The induction of the reverse transsulfuration pathway by bacterial pathogens can be considered an unrecognized mechanism for immune escape.</p><p><strong>IMPORTANCE:</strong> Macrophages are professional immune cells that ingest and kill microbes. In this study, we show that different pathogenic bacteria induce the expression of cystathionine γ-lyase (CTH) in macrophages. This enzyme is involved in a metabolic pathway called the reverse transsulfuration pathway, which leads to the production of numerous metabolites, including cystathionine. Phagocytized bacteria use cystathionine to better survive in macrophages. In addition, the induction of CTH results in dysregulation of the metabolism of polyamines, which in turn dampens the proinflammatory response of macrophages. In conclusion, pathogenic bacteria can evade the host immune response by inducing CTH in macrophages.</p>
2020-05-15 | MTBLS696 | MetaboLights
Project description:To determine whether type O FMDV-infected macrophage can release a variety of cytokines and activate innate immune responses, we have taken systematic functional genomics studies using microarray technology on differences expression gene of FMDV-infected and FMDV-uninfected mouse monocyte macrophage (RAW264.7 cells). We examined the expression patterns of 39,430 mouse genes probes, using Agilent mouse gene expression microarray. The results showed that 2541 genes were differentially expressed after FMDV infection, with 1207 up-regulated and 1334 down-regulated. Based on our previous data, the differential regulation of genes most associate with innate immune response.
2017-03-15 | GSE96588 | GEO
Project description:Macrophages play a crucial role in the inflammatory response to the human stomach pathogen Helicobacter pylori, which infects half of the world's population and causes gastric cancer. Recent studies have highlighted the importance of macrophage immunometabolism in their activation state and function. We have demonstrated that the cysteine-producing enzyme, cystathionine g-lyase (CTH), is upregulated in humans and mice with H. pylori infection. Here we show that induction of CTH in macrophages by H. pylori promotes persistent inflammation. Cth-/- mice have reduced macrophage and T-cell activation in H. pylori-infected tissues, an altered metabolome, and decreased enrichment of immune-associated gene networks, culminating in decreased H. pylori-induced-gastritis. CTH is downstream of the proposed anti-inflammatory molecule, S-adenosylmethionine (SAM). While Cth-/- mice exhibit gastric SAM accumulation, WT mice treated with SAM did not display protection against H. pylori-induced inflammation. Instead, we demonstrate that Cth-deficient macrophages exhibit alterations in the proteome, decreased NF-kB activation, diminished expression of macrophage activation markers, and impaired oxidative phosphorylation and glycolysis. Thus, through altering cellular respiration, CTH is a key enhancer of macrophage activation contributing to a pathogenic inflammatory response that is the universal precursor for the development of H. pylori-induced gastric disease.
2022-06-14 | MTBLS2851 | MetaboLights
Project description:RATIONALE: Vaccines made from a gene-modified virus and a person’s white blood cells may make the body build an effective immune response to kill tumor cells. Biological therapies, such as Granulocyte-macrophage colony-stimulating factor (GM-CSF), may stimulate the immune system in different ways and stop tumor cells from growing. Combining different types of biological therapies may kill more tumor cells.
PURPOSE: This randomized phase II trial is studying giving vaccine therapy together with dendritic cells to see how well it works compared to giving vaccine therapy together with GM-CSF in treating patients with liver or lung metastases from colorectal cancer removed by surgery.
| 2012243 | ecrin-mdr-crc
Project description:Primary outcome(s): The clinical significance of immune and gene-expression profile in colorectal cancer
| 2659791 | ecrin-mdr-crc
Project description:Tight regulation of macrophage immune gene expression is required to fight infection without risking harmful inflammation. The contribution of RNA binding proteins (RBPs) to shaping the macrophage response to pathogens remains poorly understood. Transcriptomic analysis revealed that a member of the serine/arginine-rich (SR) family of mRNA processing factors, SRSF7, is required for optimal expression of a cohort of interferon stimulated genes (ISGs) in macrophages. Using genetic and biochemical assays, we discovered that in addition to its canonical role in regulating alternative splicing, SRSF7 drives transcription of interferon regulatory transcription factor 7 (IRF7) to promote antiviral immunity. At the Irf7 promoter, SRSF7 maximizes STAT1 transcription factor binding and RNA polymerase II elongation via cooperation with the H4K20me1 histone methyltransferase KMT5a (SET8). These studies define an unorthodox role for an SR protein in activating transcription and reveal an unappreciated RNA binding protein-chromatin network that orchestrates macrophage antiviral gene expression.
2024-07-29 | GSE239845 | GEO
Project description:Cells of the innate immune system need to interpret dynamic microenvironments and rapidly respond to sequential signals to control inflammation and infection. It is unclear how complex immune signals are encoded and decoded through a small number of transcription factors and ultimately coordinate cellular decision-making. Here, we use single live cell analysis and ATAC sequencing to show that sequential inflammatory signals via the NFκB network induce memory through reprogramming of signaling network state and chromatin accessibility in primary macrophages. We use transcriptomic profiling and deep learning to show that these regulatory modes combine to explain macrophage decision-making in response to new inflammatory signals. Macrophage response to prior stimulus predicts memory state and transcriptional response to subsequent stimulus. Surprisingly, we find that innate immune memory is mediated via intracellular individual-cell factors and not via paracrine signaling between macrophages. This work comprehensively profiles the dynamic regulation of signaling networks and chromatin accessibility and their role in tuning macrophage responses to evolving inflammatory signals.
2025-03-14 | GSE261647 | GEO
Project description:Macrophage Gene Expression
| EGAD00010000448 | EGA