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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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NRROS negatively regulates ROS in phagocytes during host defense and autoimmunity

ABSTRACT: Production of reactive oxygen species (ROS) is one of the important antimicrobial mechanisms of phagocytic cells. Enhanced oxidative burst requires these cells to be primed with agents such as IFNg and LPS with a synergistic effect of these agents on the level of the burst. However, excessive ROS generation will lead to tissue damage and has been implicated in a variety of inflammatory and autoimmune disease. Therefore, this process needs to be tightly regulated. In order to understand the genes regulating this process, we will treat bone marrow derived macrophages with above mentioned priming agents and study the gene expression. We used microarrays to determine the changes in gene expression that occur in bone marrow derived macrophages after treatment with IFNg, LPS, or a combination of IFNg and LPS. Four condition experiment; Biological replicates: four replicates per condition

ORGANISM(S): Mus musculus

SUBMITTER: Jason Hackney

PROVIDER: E-GEOD-53986 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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NRROS negatively regulates ROS in phagocytes during host defense and autoimmunity

Project description:Production of reactive oxygen species (ROS) is one of the important antimicrobial mechanisms of phagocytic cells. Enhanced oxidative burst requires these cells to be primed with agents such as IFNg and LPS with a synergistic effect of these agents on the level of the burst. However, excessive ROS generation will lead to tissue damage and has been implicated in a variety of inflammatory and autoimmune disease. Therefore, this process needs to be tightly regulated. In order to understand the genes regulating this process, we will treat bone marrow derived macrophages with above mentioned priming agents and study the gene expression. We used microarrays to determine the changes in gene expression that occur in bone marrow derived macrophages after treatment with IFNg, LPS, or a combination of IFNg and LPS

2014-03-31 | GSE53986 | GEO

RNA-seq of non-LPS treated (N), non-tolerized (NT), and tolerized (T) IFNg-primed macrophages pretreated with or without HDAC3i

Project description:In this experiment we investigated the effect of HDAC3 inhibition on the transcriptome of IFNg-primed macrophages under different tolerization conditions. Peripheral blood mononuclear cells (PBMCs) were isolated from 3 healthy donors. PBMCs were isolated from whole blood of healthy donors using Ficoll gradient (Invitrogen). Monocytes (CD14+ cells) were positively selected from PBMCs using CD14 Microbeads according to the manufacturer’s instructions (Miltenyi Biotec). Monocytes were subsequently treated with or without 500 nM HDAC3i (ITF3100) for 30 minutes prior to overnight IFNg priming (50 ng/mL). Cells were then kept without LPS (non-LPS; N), treated with 10 ng/mL LPS once (non-tolerized; NT), or treated with LPS twice (tolerized; T; second LPS concentration: 100 ng/mL).

2020-02-12 | E-MTAB-8784 | biostudies-arrayexpress

Emodin inhibits macrophage classical activation [Control-LPS-IFNg-Emodin]

Project description:In order to fully characterize emodin's effects on macrophage activation, peritoneal macrophages were stimulated with LPS+IFNg with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IFNg/LPS induced changes in a large percentage of responsive genes (31%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M1 macrophage activation including: TNF, IL6, IL1b, iNOS, MMP2, and MMP9. Three-condition, one-color experiment: Vehicle control, LPS-IFNg or LPS-IFNg-Emodin treated periferal WBC PMN samples: 4 biological replicates each.

2016-07-04 | E-GEOD-73310 | biostudies-arrayexpress

Phagosome proteome of activated murine macrophage

Project description:Proteomics of carboxylated polystyrene bead (1.0 um) phagosomes from murine bone marrow-derived macrophages. cells were either resting or treated with 100 U/ml IFN-γ (PeproTech) and 100 ng/ml LPS (Sigma) for 24 h, 20 ng/ml Interleukin-4 (IL4) (BD Pharmingen) for 48 h, 20 ng/ml Interleukin-13 (IL13), 10 ng/ml Interleukin-10 (IL10)for 48 h or Reprogrammed (IL4 was incubated with BMDMs for 24 h, and the medium was replaced with fresh medium containing IFN-γ/LPS to incubate for another 24 h). Phagosomes were isolated after 30 min bead inoculation.

2019-03-22 | PXD004520 | Pride

Itaconate links inhibition of succinate dehydrogenase with macrophage metabolic remodeling and regulation of inflammation

Project description:Remodeling of the tricarboxylic acid (TCA) cycle is a metabolic adaptation mechanism accompanying inflammatory macrophage activation. During this process, endogenous metabolites can adopt regulatory roles that govern specific aspects of inflammatory response, as recently shown for succinate, which regulates the downstream pro-inflammatory IL-1Î²-HIF1a axis. Itaconate is one of the most highly induced metabolites in activated macrophages, yet its functional significance remains unknown. Here, we show that itaconate modulates macrophage metabolism and effector functions via its effect on succinate dehydrogenase, by inhibiting conversion of succinate to fumarate. Through this action, itaconate exerts anti-inflammatory effects when administered in vitro and in vivo during macrophage activation and ischemia-reperfusion injury. Using newly generated Irg1-/- mice, which lack the ability to produce itaconate, we show that endogenous itaconate regulates succinate levels and function, changes in mitochondrial respiration, and inflammatory cytokine production during macrophage activation. These studies highlight itaconate as a major physiological regulator of the global metabolic rewiring and effector functions of inflammatory macrophages. Experiment 1: mature WT BMDM were treated for 12h with 0.25 mM dimethyl itaconate (DI) or vehicle (Unst) and then stimulated with LPS (E. coli 0111:B4; 100 ng/ml, 4h) (DI+LPS; LPS); Experiment 2: mature Irg1-/- BMDM were stimulated with LPS (E. coli 0111:B4; 100 ng/ml) and murine recombinant IFNg (50 ng/ml) for 24h.

2016-07-01 | E-GEOD-82043 | biostudies-arrayexpress

Next Generation Sequencing and Quantitative Analysis of Wild Type and p110gamma-/- macrophages

Project description:Purpose: The goals of this study were to identify quantitative gene expression differences between macrophages derived from wild type and PI3Kgamma null macrophages Methods: mRNA profiles of MCSF, IL4 and IFNg/LPS stimulated macrophage wild-type (WT) and PI3Kinase gamma knockout (p110g-/-) mice were generated by single read deep sequencing, in triplicate, using Illumina HiSeq2000. The sequence reads that passed quality filters were aligned to mouse transcriptome using the bowtie2 aligner. Gene-level summaries were normalized and analyzed for differential expression using DESeq. qRTâPCR validation was performed using SYBR Green assays. Conclusions: Our study represents the first detailed analysis of the role of p110g in the control of the macrophage immune response, with biological replicates, generated by RNA-seq technology. mRNA profiles of wild type (WT) and p110g-/- macrophages were generated by deep sequencing, in triplicate, using Illumina HiSeq2000.

2016-07-18 | E-GEOD-58318 | biostudies-arrayexpress

High-throughput integration of metabolic and transcriptional profiles reveals major metabolic regulators of macrophage polarization

Project description:Macrophages polarize to divergent functional phenotypes depending on their microenvironment in a highly coordinated process of metabolic and transcriptional rewiring that is still poorly understood. We developed an Integrated Metabolomics and Gene Expression (IMAGE) profiling and analysis pipeline and applied it to extensively characterize global metabolic programs of macrophage polarization. IMAGE analysis identified 7 major (novel and known) regulatory modules responsible for metabolic rewiring during polarization, which we validated through extensive carbon and nitrogen labeling experiments. M1-specific modules included: inflammatory variant of the aspartate-arginosuccinate shunt; TCA cycle break at Idh expression accompanied by citrate accumulation and production of itaconate and fatty acid synthesis. In M2 macrophages we discovered significant role of glutamine in polarization, providing nitrogen for UDP-GlcNAc synthesis. Consistently, glutamine deprivation results in significant M2-specific defect in polarization. Our data provide, for the first time, a global view of the integrated transcriptional and metabolic changes that result in M1 and M2 polarization. Bone-marrow derived macrophages were generated from C57BL/6 mice were plated at ~100k cells per well in 96-well plate and stimulated with either Il4 or combination of LPS&IFNg or left unstimulated for 24 h mRNA was derived from lysates using Invitrogen oligo-dT beads

2014-05-30 | E-GEOD-53053 | biostudies-arrayexpress

Bone marrow-derived macrophage responses to classical activation: wild-type vs. MLL1-deficient (Lys2Cre MLL1 fx/fx)

Project description:mRNA from wild-type (Cre-) and MLL1-deficient (Cre+) BMDMs were analyzed via gene chip (Mouse Gene ST 2.1, Affymetrix) for relative expression changes. Isolated mRNA from Cre- and Cre+ BMDMs stimulated with classical activation signals (IFNg, LPS or IFNg+LPS) was analyzed using a gene chip panel of >40,000 RefSeq transcripts, and resulting fold expression was determined by analyzing quality-controlled expression values for validated probesets. Bone marrow derived macrophages from wild-type (Cre-) or MLL1-deficient (Cre+) mice were stimulated in vitro with IFNgamma (10 ng/ml), LPS (100 ng/ml) or the combination of IFNgamma+LPS for six hours. Cells were then processed in Trizol reagent for RNA extraction.

2016-06-02 | E-GEOD-82109 | biostudies-arrayexpress

Expression data from RAW 264.7 macrophage

Project description:IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine. We determined that adenosine suppressed the expression of many IFNg-regulated pro-inflammatory cytokines, chemokines, and other pro-atherogenic genes. Keywords: treatment response RAW 264.7 cells were treated for 4 hours with either IFNg or IFNg plus adenosine. Following treatment, total RNA was extracted and treatment groups were pooled from 2 separate experiments for hybridization of Affymetrix microarrays.

2009-12-30 | E-GEOD-14612 | biostudies-arrayexpress

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

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