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5,978 results for “Macrophage”
Vizgen MERFISH files for Single-cell analysis reveals M. tuberculosis ESX-1-mediated accumulation of anti-inflammatory macrophages in infected mouse lungs
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Single-cell analysis reveals M. tuberculosis ESX-1-mediated accumulation of anti-inflammatory macrophages in infected mouse lungs
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Modeling single-cell heterogeneity in signaling dynamics of macrophages reveals principles of information transmission
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Single-cell profiling identifies ACE+ granuloma macrophages as a non-permissive niche for intracellular bacteria during persistent Salmonella infection
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Human memory CD4+ T cells recognize <em>Mycobacterium tuberculosis</em>-infected macrophages amid broader pathogen-specific responses
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Phagocytosis of E. coli bacteria by macrophages
<p>Holotomography imaging of RAW 264.7 murine macrophages phagocytosing E. coli bacteria; performed in the Meijer laboratory at the Institute of Biology Leiden, Leiden University.</p> <p> </p> <p> </p>
Corrected super-resolution microscopy enables nanoscale imaging of auto-fluorescent lung macrophages
<p>Observing the cell surface and underlying cytoskeleton at nanoscale resolution using super-resolution microscopy has enabled many insights into cell signalling and function. However, the nanoscale dynamics of tissue-specific immune cells have been relatively little studied. Tissue macrophages, for example, are highly auto-fluorescent, severely limiting the utility of light microscopy. Here, we report a correction technique to remove auto-fluorescent noise from Stochastic Optical Reconstruction Microscopy (STORM) datasets. Simulations identified a moving median filter as an accurate and robust correction technique. Using this, we were able to visualise lung macrophages activated through Fc receptors by antibody-coated glass slides. Accurate, nanoscale quantification of macrophage morphology revealed that activation induced the formation of cellular protrusions tipped with MHC class I protein. These data are consistent with a role for lung macrophage protrusions in antigen presentation. We further show that the tetraspanin and extracellular vesicle (EV) marker CD81 appears in ring-shaped structures (mean diameter 93 ± 50 nm) at the surface of activated lung macrophages, likely marking the secretion of extracellular vesicles. Moreover, this correction method for super-resolution microscopy is widely applicable to other challenging biological samples.</p>
Paired human macrophage RNA sequencing data
<p>Allele-specific expression (ASE) analysis, which quantifies the relative expression of two alleles in a diploid individual, is a powerful tool for identifying <em>cis</em>-regulated gene expression variations that underlie phenotypic differences among individuals. Existing methods for gene-level ASE detection analyze one individual at a time, therefore failing to account for shared information across individuals. Failure to accommodate such shared information not only reduces power, but also makes it difficult to interpret results across individuals. However, when only RNA sequencing (RNA-seq) data are available, ASE detection across individuals is challenging because the data often include individuals that are either heterozygous or homozygous for the unobserved <em>cis</em>-regulatory SNP, leading to sample heterogeneity as only those heterozygous individuals are informative for ASE, whereas those homozygous individuals have balanced expression. To simultaneously model multi-individual information and account for such heterogeneity, we developed ASEP, a mixture model with subject-specific random effect to account for multi-SNP correlations within the same gene. ASEP only requires RNA-seq data, and is able to detect gene-level ASE under one condition and differential ASE between two conditions (e.g., pre- versus post- treatment). Extensive simulations demonstrated the convincing performance of ASEP under a wide range of scenarios. We applied ASEP to a human kidney RNA-seq dataset, identified ASE genes and validated our results with two published eQTL studies. We further applied ASEP to a human macrophage RNA-seq dataset, identified genes showing evidence of differential ASE between M0 and M1 macrophages, and confirmed our findings by results from cardiometabolic trait-relevant genome-wide association studies. To the best of our knowledge, ASEP is the first method for gene-level ASE detection at the population level that only requires the use of RNA-seq data. With the growing adoption of RNA-seq, we believe ASEP will be well-suited for various ASE studies for human diseases.</p>
Extracellular Vesicles from Pneumocystis carinii-infected rats impair fungal viability but are dispensable for macrophage functions
<p><em>Pneumocystis</em> spp. are host obligate fungal pathogens that can cause severe pneumonia in mammals and rely heavily on their host for essential nutrients. The lack of a sustainable <em>in vitro</em> culture system poses challenges in understanding their metabolism and the acquisition of essential nutrients from host lungs remains unexplored.</p> <p>Transmission electron micrographs show Extracellular Vesicles (EVs) are found near <em>Pneumocystis</em>spp. within the lung. We hypothesized that EVs transport essential nutrients to the fungi during infection. To investigate this, EVs from <em>P. carinii</em>- and <em>P. murina-</em>infected rodents were biochemically and functionally characterized. These EVs contained host proteins involved in cellular, metabolic, and immune processes as well as proteins with homologs found in other fungal EV proteomes, indicating <em>Pneumocystis</em> may release EVs. Notably, EV uptake by<em> P. carinii</em> indicated their potential involvement in nutrient acquisition and indicated a possibility for using engineered EVs for efficient therapeutic delivery. However, EVs added to <em>P. carinii</em> <em>in vitro</em>, did not show increased growth or viability, implying that additional nutrients or factors are necessary to support their metabolic requirements. Exposure of macrophages to EVs increased proinflammatory cytokine levels but did not affect macrophages' ability to kill or phagocytose <em>P. carinii</em>. These findings provide vital insights into <em>P. carinii</em> and host EV interactions, yet the mechanisms underlying <em>P. carinii</em>'s survival in the lung remain uncertain. These studies are the first to isolate, characterize, and functionally assess EVs from <em>Pneumocystis</em>-infected rodents, promising to enhance our understanding of host-pathogen dynamics and therapeutic potential.</p>
ESAT-6 undergoes self-association at phagosomal pH and an ESAT-6 specific nanobody restricts M. tuberculosis growth in macrophages
<p><em>Mycobacterium tuberculosis</em> (Mtb) is known to survive within macrophages by compromising the integrity of the phagosomal compartment in which it resides. This activity primarily relies on the ESX-1 secretion system, predominantly involving the protein duo ESAT-6 and CFP-10. CFP-10 likely acts as a chaperone, while ESAT-6 likely disrupts phagosomal membrane stability via a largely unknown mechanism. we employ a series of biochemical analyses, protein modeling techniques, and a novel ESAT-6-specific nanobody to gain insight into the ESAT-6’s mode of action. First, we measure the binding kinetics of the tight 1:1 complex formed by ESAT-6 and CFP-10 at neutral pH. Subsequently, we demonstrate a rapid self-association of ESAT-6 into large complexes under acidic conditions, leading to the identification of a stable tetrameric ESAT-6 species. Using molecular dynamics simulations, we pinpoint the most probable interaction interface. Furthermore, we show that cytoplasmic expression of an anti-ESAT-6 nanobody blocks Mtb replication, thereby underlining the pivotal role of ESAT-6 in intracellular survival. Together, these data suggest that ESAT-6 acts by a pH dependent mechanism to establish two-way communication between the cytoplasm and the Mtb-containing phagosome.</p>
Novel Macrophage Subpopulation Linked to CAD: raw and processed data files
<div> <p>This directory contains all single-cell datasets analyzed in the "Partitioning heritability using single-cell multi-omics identifies a novel macrophage subpopulation conveying increased genetic risk of coronary artery disease". Associated scripts are available at https://github.com/jhjiang2020/multiome_paper. </p> <p><strong>Jan 2025 updates</strong>: include the 10x Cell Ranger ARC output for the scATAC-seq assay. <em>Please note that 10x peaks were not used for downstream analyses. Instead, we trimmed the atac-seq fragments to retain the 9bp Tn5 cut sites at both ends and aggregated into one consensus bed file. We then recalled peaks using `MACS3 --qvalue 1e-5 --nomodel --shift -50 --extsize 100 --broad` (see discussion in https://github.com/stuart-lab/signac/issues/682). </em></p> <p> </p> </div>
Exprimental Data:Caspase-11 non-canonical inflammasome mediates the expression of proinflammatory cytokines in murine macrophages infected with leptospira interrogans.
<p>This is the exprimental data of manuscripts submitted in ALL LIFE magazine. The title is Caspase-11 non-canonical inflammasome mediates the expression of proinflammatory cytokines in murine macrophages infected with leptospira interrogans.)</p>
QPCTL regulates macrophage and monocyte abundance and inflammatory signatures in the tumor microenvironment
<p><strong>The enzyme glutaminyl-peptide cyclotransferase-like protein (QPCTL) catalyzes the formation of pyroglutamate residues at the NH<sub>2</sub>-terminus of proteins, thereby influencing their biological properties. A number of studies have implicated QPCTL in the regulation of chemokine stability. Furthermore, QPCTL activity has recently been shown to be critical for the formation of the high affinity SIRPa binding site of the CD47 “don’t-eat-me” protein. Based on the latter data, interference with QPCTL activity—and hence CD47 maturation—may be proposed as a means to promote anti-tumor immunity. However, the pleiotropic activity of QPCTL makes it difficult to predict the effects of QPCTL inhibition on the tumor microenvironment (TME). Using a syngeneic mouse melanoma model, we demonstrate that QPCTL deficiency alters the intra-tumoral monocyte-to-macrophage ratio, results in a profound increase in the presence of pro-inflammatory cancer-associated fibroblasts (CAFs) relative to immunosuppressive TGF-b1-driven CAFs, and leads to an increased IFN and decreased TGF-b transcriptional response signature in tumor cells. Importantly, the functional relevance of the observed TME remodeling is demonstrated by the synergy between QPCTL deletion and anti PD-L1 therapy, sensitizing an otherwise refractory melanoma model to anti-checkpoint therapy. Collectively, these data provide support for the development of strategies to interfere with QPCTL activity as a means to promote tumor-specific immunity.</strong></p>
An optimized 4C-seq protocol based on cistrome and epigenome data in the mouse RAW264.7 macrophage cell line
<p>In this protocol, we describe the 4C-seq method in detail using RAW264.7 cells, a mouse macrophage cell line widely used to study acute and metabolic inflammation. We specifically outline how cistrome and epigenome data can be integrated into the primer designing step, critical for the entire protocol. Because intra-TAD chromatin loops are facilitated by transcription factors and coregulators, many of which are co-localized in open chromatin regions, the binding centers of those factors can be obtained by chromatin immunoprecipitation sequencing (ChIP-seq). The binding sites of these factors reflect the coherent loci of the chromatin loops and therefore can be used as references to improve the accuracy of the 4C primers. We specifically describe the 4C protocol using examples of recently identified Ccl2 enhancer and silencer as bait. <br> </p>
Fig. 1 in Macrophages And Pigment Cells In The Liver Of Pelophylax Ridibundus (Anura)
Fig. 1. Pigment cells on the smears of the frog lake liver. Coloring according to Pappenheim. x900.
Dataset for the manuscript: Modelling the within-host spread of SARS-CoV-2 infection, and the subsequent immune response, using a hybrid, multiscale, individual-based model. Part I: Macrophages.
<p>Dataset for the manuscript:</p> <p>Modelling the within-host spread of SARS-CoV-2 infection, and the subsequent immune response, using a hybrid, multiscale, individual-based model. Part I: Macrophages. preprint, bioRxiv, 2022. DOI: 10.1101/2022.05.06.490883</p> <p>Each zip file contains the raw computational data (as a gzip compressed tarball), YAML input files, as well as Python plotting scripts. The Python plotting scripts have dependencies on the packages: <em>tarfile</em>, <em>multiprocessing</em>, <em>numpy</em>, <em>scipy</em>, and <em>matplotlib</em>. Note that the Python plotting scripts plot directly from the gzip compressed tarballs.</p> <p>The corresponding code can be found on GitHub: https://github.com/Ruth-Bowness-Group/CAModel</p>
Dataset related to article "'Understanding fibrosis pathogenesis via modelling macrophage-fibroblast interplay in immune-metabolic context"
<p>This record contains raw data related to article “ 'Understanding fibrosis pathogenesis via modelling macrophage-fibroblast interplay in immune-metabolic context"</p> <p>Abstract not avaible at the moment</p>
Macrophage targeting of nitazoxanide-loaded transethosomal gel in cutaneous leishmaniasis
<p>Topical delivery is preferable over systemic delivery for cutaneous leishmaniasis (CL), because of its easy administration, reduced systemic adverse effects, and low cost. Nitazoxanide (NTZ) has broad-spectrum activity against various parasites and has the potential to avoid drug resistance developed by enzymatic mutations. NTZ oral formulation is being associated with severe dyspepsia and stomach pain. Herein, NTZ-transethosomes (NTZ-TES) were prepared and loaded into chitosan gel (NTZ-TEG) for topical delivery. NTZ-TES were prepared by thin-film-hydration method and optimized statistically via Box-Behnken method. The optimized formulation indicated excellent particle size (176 nm), PDI (0.093), zeta potential (-26.4 mV) and entrapment efficiency (EE, 86%). The TEM analysis showed spherical sized particles and FTIR analysis indicated no interaction among the excipients. Similarly, NTZ-TEG showed optimal pH, desirable viscosity and good spreadability. NTZ-TES and NTZ-TEG showed prolonged release behavior and higher skin penetration and deposition in epidermal/dermal layer of skin in comparison with the NTZ-dispersion. Moreover, NTZ-TES showed higher percentage inhibition, lower IC50 against promastigotes and higher macrophage uptake. Additionally, skin irritation and histopathology studies indicated the safe and non-irritant behavior of the NTZ-TEG. The obtained findings suggested the enhanced skin permeation and improved anti-leishmanial effect of NTZ when administered as NTZ-TEG.</p>
Supplementary information for: Macrophage- and CD4+ T cell-derived SIV differ in glycosylation, infectivity, and neutralization sensitivity
<p>The human immunodeficiency virus (HIV) envelope protein (Env) mediates viral entry into host cells and is the primary target for the humoral immune response. Env is extensively glycosylated, and these glycans shield underlying epitopes from neutralizing antibodies. The glycosylation of Env is influenced by the type of host cell in which the virus is produced. Thus, HIV is distinctly glycosylated by CD4<sup>+</sup> T cells, the major target cells, and macrophages. However, the specific differences in glycosylation between viruses produced in these cell types have not been explored at the molecular level. Moreover, it remains unclear whether the production of HIV in CD4<sup>+</sup> T cells or macrophages affects the efficiency of viral spread and resistance to neutralization. To address these questions, we employed the simian immunodeficiency virus (SIV) model. Glycan analysis implied higher relative levels of oligomannose-type <em>N</em>-glycans in SIV from CD4<sup>+</sup> T cells (T-SIV) compared to SIV from macrophages (M-SIV), and the complex-type <em>N</em>-glycans profiles seem to differ between the two viruses. Notably, M-SIV demonstrated greater infectivity than T-SIV, even when accounting for Env incorporation, suggesting that host cell-dependent factors influence infectivity. Further, M-SIV was more efficiently disseminated by HIV-binding cellular lectins. We also evaluated the influence of cell type-dependent differences on SIV's vulnerability to carbohydrate-binding agents (CBAs) and neutralizing antibodies. T-SIV demonstrated greater susceptibility to mannose-specific CBAs, possibly due to its elevated expression of oligomannose-type <em>N</em>-glycans. In contrast, M-SIV exhibited higher susceptibility to neutralizing sera in comparison to T-SIV. These findings underscore the importance of host cell-dependent attributes of SIV, such as glycosylation, in shaping both infectivity and the potential effectiveness of intervention strategies.</p>
Monitoring melanoma patients on treatment reveals a distinct macrophage population driving targeted therapy resistance
<p><span>Resistance to targeted therapy remains a major clinical challenge in melanoma patients. To uncover resistance mechanisms, we performed single cell RNA sequencing of fine needle aspirates from resistant and responding tumors from melanoma patients before and during BRAFi/MEKi treatment. Among the genes most differentially expressed between malignant cells from resistant vs. responding tumors was POSTN encoding the secreted factor periostin. POSTN was predicted to predominantly signal to a macrophage population associated with targeted therapy resistance (TTR). Accordingly, tumors from patients with fast disease progression after targeted therapy exhibited high POSTN expression levels as well as high numbers of TTR macrophages, and POSTN was able to polarize macrophages towards a TTR phenotype. In a mouse model in vivo, POSTN expression protected melanoma from targeted therapy, which was associated with a phenotype change of intratumroal macrophages. Finally, polarized TTR macrophages protected melanoma cells from MEKi-induced killing through CD44 receptor expression on melanoma cells. Thus, interfering with the protective activity of TTR macrophages might represent a strategy to overcome resistance to targeted therapy in melanoma.</span></p>
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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.