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Epigenetic profiling of mouse bone marrow derived mast cells (BMMCs) [ChIP-seq]

ABSTRACT: Allergy is one of the least understood immunological response partly due to the diversity of allergens and the complexity of immune response against them. In allergic responses, mast cells are key players with their ability to rapidly degranulate and also generate de novo lipids and transcripts. Although the molecular details of degranulation in mast cell were studied in allergic inflammation, the transcriptional response involving chromatin remodeling, enhancer dynamics and long non-coding RNA (lncRNA) expression are largely unexplored. Here, using mouse bone marrow derived mast cells (BMMCs), we characterized the steady state, immunoglobulin E (IgE) and antigen (Ag) mediated epigenetic changes in mast cell chromatin and described the enhancer, super-enhancer and mRNA, lncRNA catalogue in these cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE75525 | GEO | 2019/12/01

REPOSITORIES: GEO

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Transcriptomic profiling of bone marrow derived mast cells (BMMCs) [RNA-seq]

Project description:Allergy is one of the least understood immunological response partly due to the diversity of allergens and the complexity of immune response against them. In allergic responses, mast cells are key players with their ability to rapidly degranulate and also generate de novo lipids and transcripts. Although the molecular details of degranulation in mast cell were studied in allergic inflammation, the transcriptional response involving chromatin remodeling, enhancer dynamics and long non-coding RNA (lncRNA) expression are largely unexplored. Here, using mouse bone marrow derived mast cells (BMMCs), we characterized the steady state, immunoglobulin E (IgE) and antigen (Ag) mediated epigenetic changes in mast cell chromatin and described the enhancer, super-enhancer and mRNA, lncRNA catalogue in these cells.

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Gene expression profile of Pafah2-deficient bone marrow derived mast cells (BMMCs) treated with w3 epoxides or GW9662

Project description:Gene expression profile of Pafah2-deficient bone marrow derived mast cells (BMMCs) treated with w3 epoxides or GW9662

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Bone marrow-derived mast cells +- IL-33 48h

Project description:Mast cells are tissue resident granulocytes which are most abundant at the interface between tissues and the external environment, such as around blood vessels, in the skin or mucosal surfaces in the lungs and gut. Pathologically they are involved in allergic reactions and anaphylaxis, however they may also play protective roles in responses to some infections, particularly to pathogenic helminths. Mast cells also express high levels of the IL-33 receptor, which like TLRs, activates Myd88 dependent signalling pathways to drive de novo cytokine production in mast cells.IL-33 is a member of the IL-1 family known to stimulate a number of immune cell types including mast cells. IL-33 is a strong activator of de novo cytokine production in mast cells without inducing degranulation, although it has also been shown to synergise with other signals to promote degranulation. Bone Marrow-Derived Mast cells (BMMCs) were cultured as described previously [27]. Briefly, bone marrow was flushed in PBS and the cells pelleted by centrifugation. Cells were cultured at 1 million cells per ml in RPMI 1640 supplemented with 10% FBS (Biosera/Labtech), 5 mM l‐Glutamine (GIBCO Life Technologies), 100 U/ml Penicillin (GIBCO Life Technologies), 100 μg/ml Streptomycin (GIBCO Life Technologies), 25 mM HEPES (Lonza), 1 mM sodium pyruvate (Lonza), 1X nonessential amino acids (Lonza), 50 μM 2‐mercaptoethanol and 30 ng/ml IL‐3 (PeproTech). Cells were passaged twice per week and used between passage 12 and 16. 4 independent BMMC cultures were either stimulated with 10 ng/ml IL-33 for 48 hours or left unstimulated, followed by single shot LC-MS analysis.

2023-03-11 | PXD033759 | Pride

Chronic allergen exposure drives accumulation of long-lived IgE plasma cells in the bone marrow, giving rise to serological memory

Project description:Summary: Long-lived IgE plasma cells reside in the bone marrow of allergic mice and atopic humans, confer IgE serological memory and produce allergen-specific IgE that can drive anaphylaxis. Abstract: Immunoglobulin E (IgE) plays an important role in allergic diseases. Nevertheless, the source of IgE serological memory remains controversial. We re-examined the mechanism of serological memory in allergy using a dual-reporter system to track IgE plasma cells (PCs) in mice. Short-term allergen exposure resulted in the generation of IgE plasma cells that resided mainly in secondarylymphoid organs and produced IgE that was unable to degranulate mast cells. In contrast, chronic allergen exposure led to the generation of long-lived IgE plasma cells that were primarily derived from sequential class switching of IgG1, accumulated in the bone marrow (BM) and produced IgE capable of inducing anaphylaxis. Most importantly, IgE plasma cells were found in the BM of human allergic, but not non-allergic donors, and allergen-specific IgE produced by these cells was able to induce mast cell degranulation when transferred to mice. These data demonstrate that longlived IgE BMPCs arise during chronic allergen exposure and establish serological memory in both mice and humans.

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Microarray analysis of naïve bone marrow derived mast cells (BMMCs) and BMMCs 4hr post ionomycin activation

Project description:Microarray analysis of naïve bone marrow derived mast cells (BMMCs) and BMMCs 4hr post ionomycin activation

| PRJNA854268 | ENA

Mast Cell Maturation is Driven via a Novel Group III Phospholipase A2-Prostaglandin D2-DP1 Receptor Paracrine Axis

Project description:Microenvironment-based alterations in mast cell phenotypes influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 synthase (L-PGDS) to provide PGD2, which facilitates mast cell maturation via PGD2 receptor (DP1). Mice lacking PLA2G3, L-PGDS or DP1, mast cell-deficient mice reconstituted with PLA2G3- or DP1-null mast cells, or mast cells cocultured with L-PGDS-ablated fibroblasts exhibited impaired mast cell maturation and anaphylaxis. Thus, we describe a lipid-driven PLA2G3-L-PGDS-DP1 loop that drives mast cell maturation. Mast cell maturation; immature and mature bone marrow-derived mast cells (BMMCs); Four-condition experiment (mature BMMCs vs immature BMMCs, Pla2g3M-bM-^@M-^S/M-bM-^@M-^S vs Pla2g3+/+); 3 replicates of Pla2g3+/+ BMMCs, 4 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S BMMCs, 4 replicates of Pla2g3+/+ cocultured BMMCs, 3 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S cocultured BMMCs

2013-03-09 | E-GEOD-44980 | biostudies-arrayexpress

Microarray analysis of naïve bone marrow derived mast cells (BMMCs) and BMMCs 4hr post ionomycin activation

Project description:Gene expression profile of BMMCs four hours post activation with ionomycin compared to naive BMMCs.

2022-09-27 | GSE207235 | GEO

Murine bone marrow-derived mast cells (BMMCs) transduced with pAPM lentiviruses overexpressing miR-221 vs control overexpressing miR-221m.

Project description:Bone marrow-derived mast cells were derived from three different female C57Bl/6 mice of similar age. Cells were transduced with pAPM lentiviruses either overexpressing microRNA-221 or a non functional microRNA-221 mutant, termed miR-221m, where four point-mutations were introduced in the seed sequence of miR-221. The samples overexpressing miR-221m were used as references for the corresponding miR-221 overexpressing BMMCs from the same mouse (mouse matched reference). The experiment was performed in order to gain more insights about the molecular mechanisms underlying miR-221 effects in mast cells. Two-condition experiment, BMMC overexpressing miR-221 vs BMMC overexpressing miR-221m. Biological replicates: 3 replicates overexpressing miR-221, 3 control replicates overexpressing miR-221m.

2011-11-23 | E-GEOD-24462 | biostudies-arrayexpress

Transcriptional heterogeneity of mast cells and basophils upon activation.

Project description:Mast cells and basophils are developmentally related cells whose activation is a hallmark of allergy. Functionally, mast cells and basophils overlap in their ability to produce several mediators, including histamine and granule proteases, but studies have increasingly demonstrated non-redundant roles. To characterize the transcriptional heterogeneity of mast cells and basophils upon their activation, we performed large-scale comparative microarrays of murine bone marrow–derived mast cells (BMMCs) and basophils (BMBs) at rest, upon an adaptive-type activation (IgE crosslinking), or upon an innate-type activation (IL-33 stimulation). Hierarchical clustering demonstrated that BMMCs and BMBs shared specific activation-associated transcriptional signatures but differed in others, both between cell type and between activation mode. In BMMCs, IgE crosslinking upregulated 785 genes including Egr2, Ccl1, and Fxyd6, while IL-33 stimulation induced 823 genes including Ccl1, Egr2, and Il1b. Focused bioinformatics pathway analysis demonstrated that IgE activation aligned with processes such as oxidative phosphorylation, angiogenesis, and the p53 pathway. The IL-33–activated transcriptome was enriched in genes commonly altered by NF-B in response to TNF, by IL-6 via STAT3, and in response to IFN. Furthermore, BMBs activated via IgE crosslinking selectively induced immune response genes Ccl1, Il3, and Il2 compared to IL-33–stimulated BMBs. Principal-component analysis revealed key cell- and activation-specific clustering. Overall, our data demonstrate that mast cells and basophils have cell- and activation-specific transcriptional responses and suggest that context-specific gene networks and pathways may shape how the immune system responds to allergens and innate cytokines.

2017-03-17 | GSE96696 | GEO

Effect of deficiency of Elk4 on transcriptome changes in murine bone marrow derived mast cells upon FcϵRI mediated activation

Project description:The proliferative potential of mast cells after activation for 3-4h was found to be decreased, which suggests that mast cell degranulation and cell proliferation are differentially regulated. ELK4, a member of the ternary complex factor (TCF) subfamily of Ets transcription factors, is one of the downstream effectors of MAPK signaling that is critical for cell proliferation. And Elk4 has been identified to be vital for macrophage activation in response to zymosan and the transcriptional response to 12-O-tetrade canoyl phorbol-13-acetate (TPA) stimulation in fibroblast. However, the effect of ELK4 on the mast cell transcriptional response to FcϵRI and GPCR mediated activation and its potential functional significance in mast cells remain unclear. Here, We characterised the transcriptional program downstream of FcϵRI signalling using IgE-DNP/HSA stimulation by RNA-seq. The investigation of the transcriptional response was performed using murine bone marrow derived mast cells(BMMCs) from different animals: (i) wild type mice, (ii) Elk4 heterozygous mice, (iii) Elk4 knockout mice. Overall, our study identifies a new physiological role of the transcription factor ELK4 in mast cell proliferation and activation.

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