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5,978 results for “Macrophages”
Data from: Transcriptional profiling of lung macrophages following ozone exposure in mice identifies signaling pathways regulating immunometabolic activation
<p>Macrophages play a key role in ozone-induced lung injury by regulating both the initiation and resolution of inflammation. These distinct activities are mediated by pro-inflammatory and anti-inflammatory/pro-resolution macrophages which sequentially accumulate in injured tissues. Macrophage activation is dependent, in part, on intracellular metabolism. Herein, we used RNA-sequencing (seq) to identify signaling pathways regulating macrophage immunometabolic activity following exposure of mice to ozone (0.8 ppm, 3 hr) or air control. Analysis of lung macrophages using an Agilent Seahorse showed that inhalation of ozone increased macrophage glycolytic activity and oxidative phosphorylation at 24 and 72 hr post exposure. An increase in the percentage of macrophages in the S phase of the cell cycle was observed 24 hr post ozone. RNA-seq revealed significant enrichment of pathways involved in innate immune signaling and cytokine production among differentially expressed genes at both 24 and 72 hr after ozone, while pathways involved in cell cycle regulation were upregulated at 24 hr and intracellular metabolism at 72 hr. An interaction network analysis identified tumor suppressor 53 (TP53), E2F family of transcription factors (E2Fs), Cyclin Dependent Kinase Inhibitor 1A (CDKN1a/p21), and Cyclin D1 (CCND1) as upstream regulators of cell cycle pathways at 24 hr and TP53, nuclear receptor subfamily 4 group a member 1 (NR4A1/Nur77), and estrogen receptor alpha (ESR1/ERα) as central upstream regulators of mitochondrial respiration pathways at 72 hr. These results highlight the complex interaction between cell cycle, intracellular metabolism, and macrophage activation which may be important in the initiation and resolution of inflammation following ozone exposure.</p>
Processed read counts from macrophage RNA-seq and ATAC-seq experiments
<p><strong>RNA-seq files:</strong></p> <ol> <li>RNA_count_matrix.txt.gz - raw read counts</li> <li>RNA_cqn_matrix.txt.gz - read counts quantile normalised with the cqn R package</li> <li>RNA_gene_metadata.txt.gz - information about the genes</li> <li>RNA_sample_metadata.txt.gz - information about the samples</li> </ol> <p><strong>ATAC-seq files:</strong></p> <ol> <li>ATAC_count_matrix.txt.gz - raw read counts</li> <li>ATAC_cqn_matrix.txt.gz - read counts quantile normalised with the cqn R package</li> <li>ATAC_peak_metadata.txt.gz - peak coordinates and other metadata</li> <li>ATAC_sample_metadata.txt.gz - sample metadata</li> <li>ATAC_consensus_peaks.gff3.gz - GFF3 file containing the GRCh38 coordinates of the peaks</li> </ol>
Gene expression QTL lead variants in macrophages stimulated with IFNg and Salmonella
<p>Lead eQTL variants from RASQUAL and FastQTL analyses.</p> <p>Columns in the RASQUAL results:</p> <ul> <li>snp_id - id of the lead eQTL variant</li> <li>gene_id - id of the gene</li> <li>chisq - Chi-square statistics from RASQUAL</li> <li>p_nominal - Nominal p-value from RASQUAL</li> <li>p_eigen - Nominal p-value corrected by EigenMT for the number of indepedent tests in the cis region of the gene.</li> <li>n_tests - Number of independent tests estimated by EigenMT</li> <li>fdr_thresh - Empirical FDR 10% threshold. Those eQTLs for which p_eigen < fdr_threshold are significant at the 10% FDR level.</li> </ul> <p> </p>
Summary statistics of transcript usage QTLs in naive and stimulated macrophages (part 2)
<p>Column names:</p> <ol> <li>phenotype_id</li> <li>pheno_chr</li> <li>pheno_start</li> <li>pheno_end</li> <li>strand - strand of the phenotype</li> <li>n_snps - number of SNPs tested per phenotype</li> <li>distance - distance from the variant to the phenotype</li> <li>snp_id</li> <li>snp_chr</li> <li>snp_start - position of the SNP</li> <li>snp_end - same as snp_start</li> <li>p_nominal - nominal p-value from QTLTools</li> <li>beta - effect size from QTLTools</li> <li>is_lead - is the variant the lead QTL for the phenotype?</li> </ol>
Summary statistics of transcript usage QTLs in naive and stimulated macrophages (part 1)
<p>Column names:</p> <ol> <li>phenotype_id</li> <li>pheno_chr</li> <li>pheno_start</li> <li>pheno_end</li> <li>strand - strand of the phenotype</li> <li>n_snps - number of SNPs tested per phenotype</li> <li>distance - distance from the variant to the phenotype</li> <li>snp_id</li> <li>snp_chr</li> <li>snp_start - position of the SNP</li> <li>snp_end - same as snp_start</li> <li>p_nominal - nominal p-value from QTLTools</li> <li>beta - effect size from QTLTools</li> <li>is_lead - is the variant the lead QTL for the phenotype?</li> </ol>
Development of an imaging toolbox to assess the therapeutic potential and biodistribution of macrophages in a mouse model of multiple organ dysfunction
<p>Data set to accompany manuscript entitled "Development of an imaging toolbox to assess the therapeutic potential and biodistribution of regenerative therapies in a mouse model of multiple organ dysfunction " which can be found on BioRxiv.</p>
Macrophage Secreted TGF-β1 Contributes to Fibroblast Activation and Ureteral Stricture Following Ablation Injury
<p>Original dataset for figures.</p>
Serum response factor utilizes distinct promoter- and enhancer-based mechanisms to regulate cytoskeletal gene expression in macrophages.
<p>Cells of the monocyte/macrophage lineage play essential roles in tissue homeostasis and immune responses, but mechanisms underlying the coordinated expression of cytoskeletal genes required for specialized functions of these cells, such as directed migration and phagocytosis, remain unknown. Here, using genetic and genomic approaches, we provide evidence that serum response factor (SRF) regulates both general and cell type-restricted components of the cytoskeletal gene expression program in macrophages. Genome-wide location analysis of SRF in macrophages demonstrates enrichment of SRF binding at ubiquitously expressed target gene promoters, as expected, but also reveals that the majority of SRF binding sites associated with cell type-restricted target genes are at distal inter- and intragenic locations. Most of these distal SRF binding sites are established by the prior binding of the macrophage- and the B cell-specific transcription factor PU.1 and exhibit histone modifications characteristic of enhancers. Consistent with this, representative cytoskeletal target genes associated with these elements require both SRF and PU.1 for full expression. These findings suggest that SRF uses two distinct molecular strategies to regulate programs of cytoskeletal gene expression: a promoter-based strategy for ubiquitously expressed target genes and an enhancer-based strategy at target genes that exhibit cell type-restricted patterns of expression.</p>
Data from: Panderodus from the Waukesha lagerstätte of Wisconsin, USA: the anatomy of primitive macrophagous vertebrate predators
<p>Conodonts are an extinct group of early vertebrates. Articulated fossils of their feeding apparatus ('natural assemblages') are rare, and preserved soft tissues vanishingly so. Here, a primitive conodont with preserved soft tissues is redescribed from the Waukesha Lagerstätte of Wisconsin, USA. Although the feeding apparatus of derived prioniodontid conodonts is well understood, together with the homologies between taxa, the same is not true of more primitive conodonts that have apparatuses composed entirely of coniform elements. The new data provide insight to the long-term problem of determining homology across different types of conodont feeding apparatus. The Waukesha <i>Panderodus</i> preserves an almost complete apparatus and comprises two parallel rows of elements that occluded across the sagittal plane. A pair of M elements lies at the rostral end of the apparatus, with four pairs of S elements located immediately caudal to them. Three pairs of P elements are identified at the caudal end of the apparatus, for the first time in a primitive conodont with coniform elements. A symmetrical S<sub>0</sub> element is located on the midline between the M–S and P suites and provides the key for establishing homology with more derived ramiform–pectiniform apparatuses. The exceptional preservation reveals cartilaginous supports for the elements that inserted into their basal cavities. The trunk of the animal is poorly preserved but was dorso-ventrally flattened in life with transverse myomeres containing muscle fibrils. Overall, the specimen shows that <i>Panderodus</i> was a macrophagous feeder and provides an insight to the functional anatomy of early vertebrate predation.</p>
Nontuberculous mycobacteria persistence in a cell model mimicking alveolar macrophages (genome assembly and annotation dataset)
<p>This dataset includes the assembled contigs (.fasta and .gbk files), the nucleotide sequences of the prediction transcripts (CDS, rRNA, tRNA, tmRNA, misc_RNA) (.ffn files) and the respective amino acid sequences of the translated CDS sequences (.faa files) for the following Nontuberculous mycobacteria (NTM) strains: <em>Mycobacterium smegmatis </em>mc<sup>2</sup>155 (reference strain), <em>Mycobacterium avium</em> ATCC25921 (reference strain), <em>M. avium </em>60/08 (clinical strain), <em>Mycobacterium fortuitum</em> ATCC6841 (reference strain) and <em>M. fortuitum</em> 747/08 (clinical strain).</p> <p>All raw sequence reads used in this study were deposited in the European Nucleotide Archive (ENA) (BioProject PRJEB30455).</p> <p>The associated article can be found here: <a href="https://www.ncbi.nlm.nih.gov/pubmed/31035520">https://www.ncbi.nlm.nih.gov/pubmed/31035520</a></p> <p> </p>
Macrophage fumarate hydratase restrains mtRNA-mediated interferon production
<p>Metabolic rewiring underlies macrophage effector functions, but the mechanisms involved remain incompletely defined. Here, using unbiased metabolomics and stable isotope-assisted tracing, we show induction of an inflammatory aspartate-argininosuccinate shunt following LPS stimulation. The shunt, supported by increased ASS1 expression, also leads to increased cytosolic fumarate levels and fumarate-mediated protein succination. Pharmacologic inhibition and genetic ablation of the TCA cycle enzyme FH further elevates intracellular fumarate levels, suppresses mitochondrial respiration, and increases mitochondrial membrane potential. RNA sequencing and proteomic analysis demonstrate profound inflammatory effects resulting from FH inhibition. Of note, acute FH inhibition suppresses IL-10 expression leading to increased TNF-α secretion, an effect recapitulated by fumarate esters. Unexpectedly, FH inhibition, but not fumarate esters, also increases IFN-β production through mechanisms that are driven by mitochondrial RNA (mtRNA) release and activation of the RNA sensors TLR7 and RIG-I/MDA5. This effect is recapitulated endogenously when FH is suppressed following prolonged LPS stimulation. Furthermore, cells from SLE patients also exhibit FH suppression, indicating a potential pathogenic role for this process in human disease. We therefore identify a protective role for FH in maintaining appropriate macrophage cytokine and interferon responses.</p> <p>Data from this study that is included in this Dryad submission is as follows:</p> <p>1. RNA sequencing of non-stimulated (with vehicle DMSO) or lipopolysaccaharide-stimulated (4 h) murine bone marrow-derived macrophages (BMDMs) pre-treated with vehicle (DMSO), 20 micromolar fumarate hydratase inhibitor 1 (FHIN1) or 25 micromolar dimethylfumarate (DMF) for 3 h. Three biological replicates per condition.</p> <p>2. Label-free proteomics of lipopolysaccaharide-stimulated (4 h) murine bone marrow-derived macrophages (BMDMs) pre-treated with vehicle (DMSO), 20 micromolar fumarate hydratase inhibitor 1 (FHIN1) or 25 micromolar dimethylfumarate (DMF) for 3 h. Five biological replicates per condition. </p> <p>3. Metabolomics source data used for the study.</p>
Raw Data for the article: Cigarette smoke promotes inflammasome-independent activation of caspase-1 and -4 leading to gasdermin D cleavage in human macrophages
<p>Mechanisms and consequences of gasdermin D (GSDMD) activation in cigarette smoke (CS)-associated inflammation and lung disease are unknown. GSDMD is a downstream effector of caspase-1, -8, and -4. Upon cleavage, GSDMD generates pores into cell membranes. Different degrees of GSDMD activation are associated with a range of physiological outputs ranging from cell hyperactivation to pyroptosis. We have previously reported that in human monocyte-derived macrophages CS extract (CSE) inhibits the NLRP3 inflammasome and shifts the response to lipopolysaccharide (LPS) towards the TLR4-TRIF axis leading to activation of caspase-8, which, in turn, activates caspase-1. In the present work, we investigated whether other ASC-dependent inflammasomes could be involved in caspase activation by CSE and whether caspase activation led to GSDMD cleavage and other downstream effects. Presented results demonstrate that CSE promoted ASC-independent activation of caspase-1 leading to GSDMD cleavage and increased cell permeability, in the absence of cell death. GSDMD cleavage was strongly enhanced upon stimulation with LPS+CSE, suggesting a synergistic effect between the two stimuli. Noteworthy, CSE promoted LPS internalization leading to caspase-4 activation, thus contributing to increased GSDMD cleavage. Caspase-dependent GSDMD cleavage was associated with mitochondrial superoxide generation. Increased cleaved GSDMD was found in lung macrophages of smokers compared to ex-smokers and non-smoking controls. Our findings revealed that ASC-independent activation of caspase-1, -4, and -8 and GSDMD cleavage upon exposure to CS may contribute to macrophage dysfunction and feed the chronic inflammation observed in the smokers' lung.</p>
DRAM1 Promotes Lysosomal Delivery of Mycobacterium marinum in Macrophages
<p>Confocal RAW imaging data related to manuscript DRAM1 Promotes Lysosomal Delivery of Mycobacterium marinum in Macrophages.</p>
Data from: Crystalline silica-induced proinflammatory eicosanoid storm in novel alveolar macrophage model quelled by docosahexaenoic acid
<p>Introduction: Workplace exposure to respirable crystalline silica (cSiO<sub>2</sub>) is associated with chronic inflammatory and autoimmune diseases. At the mechanistic level, cSiO<sub>2</sub> particles are quickly phagocytosed by resident alveolar macrophages (AMs) in the lung, causing a robust cycle of proinflammatory cytokine release, lysosomal rupture, mitochondrial toxicity, and immunogenic cell death if the particle is not efficiently cleared by the lung. We and others have demonstrated in bone marrow-derived and transformed macrophage models that supplementation with the ω-3 polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) contributes to increased membrane phospholipid content of DHA and subsequent suppression of cSiO<sub>2</sub>-triggered inflammatory responses. However, mechanistic exploration of ω-3 PUFA effects in AMs is challenging due to reliance on short-lived primary AMs derived from lung lavage fluid.</p> <p>Methods: To address these limitations, we have employed a recently developed novel self-renewing AM model from C57BL/6 mice, fetal liver-derived alveolar-like macrophages (FLAMs), that is phenotypically representative of primary lung AM populations. We found that incubation of FLAMs with 25 µM DHA as ethanolic suspensions or as complexes with bovine serum albumin were equally effective at increasing ω-3 PUFA content of phospholipids at the expense of the ω-6 PUFA arachidonic acid (ARA) and the ω-9 monounsaturated fatty acid oleic acid. Based on these findings, FLAMs were treated with 25 µM DHA in EtOH or EtOH vehicle (VEH) for 24 h, with or without LPS for 2 h, and with or without cSiO<sub>2</sub> for 1.5 or 4 h then proinflammatory cytokine release, lysosomal membrane permeabilization, and mitochondrial depolarization assessed. In addition, oxylipin metabolites were measured using a targeted LC-MS lipidomics panel of 156 metabolites.</p> <p>Results: Regardless of whether FLAMs were LPS-primed, cSiO<sub>2</sub>-triggered lysosomal permeability, mitochondrial toxicity, and cell death were not impacted by DHA. LPS+cSiO<sub>2</sub> elicited marked IL-1α, IL-1β, and TNF-α release after 1.5 and 4 h of cSiO<sub>2</sub> exposure, which was significantly inhibited by DHA. In VEH-treated cells, cSiO<sub>2</sub> alone and LPS+cSiO2 induced synthesis of ARA-derived proinflammatory oxylipins including prostaglandins, leukotrienes, and thromboxanes that was suppressed by DHA. In addition, DHA promoted synthesis of pro-resolving DHA-derived oxylipins at the expense of ARA-derived oxylipins.</p> <p>Discussion: FLAMs were amenable to lipidome modulation by DHA, which suppressed cSiO<sub>2</sub>-triggered proinflammatory cytokine responses and ARA-derived oxylipins that potentially contribute to the particle's toxicity in the lung. FLAMs are a promising in vitro alternative to primary AMs for investigating interventions against toxicant-triggered inflammation and autoimmunity in the lung.</p>
Code and data for "Bordetella adenylate cyclase toxin elicits chromatin remodeling and transcriptional reprogramming that blocks differentiation of monocytes into macrophages"
<p># Code and data for "Bordetella adenylate cyclase toxin elicits chromatin remodeling and transcriptional reprogramming that blocks differentiation of monocytes into macrophages"</p> <p><br> - `pipeline` contains scripts for processing raw reads with `nf-core/rnaseq` Nextflow pipeline<br> - `setup_conda.sh` sets up a conda environment for Nextflow<br> - `samplesheet.csv` describes the samples<br> - `rna-seq-nextflow.sh` runs the analysis<br> - `data` contains the quantifications by Salmon from the pipeline and data for the CRE motif (see `analysis.Rmd` for more details)<br> - `analysis.Rmd` an R notebook containing a code to reproduce conclusions and figures in the paper and additional comments.</p> <p>The R environment (all packages) is reproducibly reconstructed via `renv` - run `renv::restore()` after loading the project.</p> <p>The generated figures and tables are stored in the `outputs` directory.</p> <p> </p>
Kupffer cell-like syncytia replenish resident macrophage function in fibrotic liver
<p class="AbstractSummary"><span>Kupffer cells (KCs) are localized in liver sinusoids but extend pseudopods to parenchymal cells to maintain their identity and serve as the body's central bacterial filter. Liver cirrhosis dramatically alters vascular architecture, but how KCs adapt is unclear. We used a mouse model of liver fibrosis and human tissue to examine immune adaptation. Fibrosis forced KCs to lose contact with parenchymal cells, downregulating "KC identity", which rendered them incapable of clearing bacteria. Commensals stimulated the recruitment of monocytes via CD44 to a spatially distinct vascular compartment. There, they formed large aggregates of multinucleated cells (syncytia) that expressed phenotypical KC markers and displayed enhanced bacterial catching ability. Syncytia formed via CD36 and were observed in human cirrhosis as a possible antimicrobial defense that evolved with fibrosis.</span></p>
SYSTEMS LEVEL IDENTIFICATION OF A MATRISOME-ASSOCIATED MACROPHAGE POLARIZATION STATE IN MULTI-ORGAN FIBROSIS
<p>This Zenodo repository contains the processed Seurat objects for "SYSTEMS LEVEL IDENTIFICATION OF A MATRISOME-ASSOCIATED MACROPHAGE POLARIZATION STATE IN MULTI-ORGAN FIBROSIS".</p> <p>The Seurat objects include:</p> <ul> <li>Tissue-specific monocytes / macrophages (used in Figure 1,3,4) <ul> <li>endo.rds: Endometrium monocytes / macrophages</li> <li>heart.rds: Heart monocytes / macrophages</li> <li>kidney.rds: Kidney monocytes / macrophages</li> <li>liver.rds: Liver monocytes / macrophages</li> <li>lung.rds: Lung monocytes / macrophages</li> <li>skin.rds: Skin monocytes / macrophages</li> </ul> </li> <li>SPP1 macrophages across all six tissues (used in Figure 2,3,4,5) <ul> <li>SPP1seu.rds</li> </ul> </li> </ul> <p>Code for generating these objects can be found at: https://github.com/the-ouyang-lab/mam-reproducibility</p>
Lipidomic data of macrophages isolated from adult fruit flies (Drosophila melanogaster) 24 hours post-infection
<p>The immune response is an energy-demanding process that must be coordinated with systemic metabolic changes redirecting nutrients from stores to the immune system. Although this interplay is fundamental for the function of the immune system, the underlying mechanisms remain elusive. </p> <p>Our data show that the pro-inflammatory polarization of <em>Drosophila</em> macrophages is coupled to the production of the insulin antagonist <em>ImpL2</em> through the activity of the transcription factor HIF1α. <em>ImpL2</em> production, reflecting nutritional demands of activated macrophages, subsequently impairs insulin signaling in the fat body, thereby triggering FOXO-driven mobilization of lipoproteins. This metabolic adaptation is fundamental for the function of the immune system and an individual's resistance to infection.</p> <p>We demonstrated that analogically to <em>Drosophila</em>, mammalian immune-activated macrophages produce <em>ImpL2</em> homolog IGFBP7 in a HIF1α-dependent manner and that enhanced IGFBP7 production by these cells induces mobilization of lipoproteins from hepatocytes.</p> <p>Hence, the production of <em>ImpL2</em>/IGFBP7 by macrophages represents an evolutionarily conserved mechanism by which macrophages alleviate insulin signaling in the central metabolic organ to secure nutrients necessary for their function upon bacterial infection.</p>
Vaccination With Autologous Breast Cancer Cells Engineered to Secrete Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) in Metastatic Breast Cancer Patients
ClinicalTrials.gov study NCT00317603. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Granulocyte-Macrophage Stimulating Factor in the Treatment of Peripheral Arterial Disease
ClinicalTrials.gov study NCT01041417. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.