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Lipid-orchestrated paracrine circuit coordinates mast cell maturation and anaphylaxis through functional interaction with fibroblasts [skin scRNA-seq]

ABSTRACT: Lipid-orchestrated paracrine circuit coordinates mast cell maturation and anaphylaxis through functional interaction with fibroblasts [skin scRNA-seq]

PROVIDER: PRJNA1092348 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28467023_1.fastq.gz	Fastqsanger.gz
	SRR28467023_2.fastq.gz	Fastqsanger.gz
	SRR28467024_1.fastq.gz	Fastqsanger.gz
	SRR28467024_2.fastq.gz	Fastqsanger.gz
	SRR28467025_1.fastq.gz	Fastqsanger.gz

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Lipid-orchestrated paracrine circuit coordinates mast cell maturation and anaphylaxis through functional interaction with fibroblasts [skin scRNA-seq]

Project description:Interaction of mast cells (MCs) with fibroblasts is essential for MC maturation within tissue microenvironments, although the underlying mechanism is incompletely understood. Through a phenotypic screening of >30 mouse lines deficient in lipid-related genes, we found that deletion of the lysophosphatidic acid (LPA) receptor LPA1, like that of the phospholipase PLA2G3, the prostaglandin D2 (PGD2) synthase L-PGDS, or the PGD2 receptor DP1, impairs MC maturation and thereby anaphylaxis. Mechanistically, MC-secreted PLA2G3 acts on extracellular vesicles (EVs) to supply lysophospholipids, which are converted by fibroblast-derived autotaxin (ATX) to LPA. Fibroblast LPA1 then integrates multiple pathways required for MC maturation by facilitating integrin-mediated MC-fibroblast adhesion, IL-33-ST2 signaling, L-PGDS-driven PGD2 generation, and feedforward ATX-LPA1 amplification. Defective MC maturation resulting from PLA2G3 deficiency is restored by supplementation with LPA1 agonists or PLA2G3-modified EVs. Thus, the lipid-orchestrated paracrine circuit involving PLA2G3-driven lysophospholipid, eicosanoid, integrin, and cytokine signaling fine-tunes MC-fibroblast communication, ensuring MC maturation.

2024-11-12 | GSE262558 | GEO

Lipid-orchestrated paracrine circuit coordinates mast cell maturation through functional interaction with fibroblasts [mast cell]

2024-11-12 | GSE253356 | GEO

Lipid-orchestrated paracrine circuit coordinates mast cell maturation through functional interaction with fibroblasts [fibroblast]

2024-11-12 | GSE253361 | GEO

Lipid-orchestrated paracrine circuit coordinates mast cell maturation through functional interaction with fibroblasts [mast cell]

Project description:Lipid-orchestrated paracrine circuit coordinates mast cell maturation through functional interaction with fibroblasts [mast cell]

| PRJNA1065395 | ENA

Lipid-orchestrated paracrine circuit coordinates mast cell maturation through functional interaction with fibroblasts [fibroblast]

Project description:Lipid-orchestrated paracrine circuit coordinates mast cell maturation through functional interaction with fibroblasts [fibroblast]

| PRJNA1065414 | 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

Effects of group III phospholipase A2 deficiency in mast cells on fibroblast-directed maturation of mast cells in vitro

2013-03-09 | GSE44980 | GEO

MAZR and mast cells

Project description:Mast cells are known to be the key players in type I hypersensitivity reactions in humans and mice. They are critically involved in the development of allergic rhinitis, allergic asthma and systemic anaphylaxis. In this study we investigated the role of the transcriptional regulator MAZR in mast cells by comparing the expression profile of mast cells generated from wild-type (MazrF/F) and MAZR-deficient (MazrF/F x Vav-iCre) bone marrow cells. Our results from the array data demonstrate that MAZR acts preferentially as a transcriptional repressor in mast cells.

2013-10-18 | E-MTAB-1816 | biostudies-arrayexpress

Stem cell factor programs the mast cell activation phenotype

Project description:Mast cells, activated by antigen via the high affinity receptor for IgE (FcεRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. Mouse bone marrow-derived mast cells were treated with IL3, IL3+IL33, or IL3+SCF. Six replicates each.

2012-05-01 | E-GEOD-35332 | biostudies-arrayexpress

Mast cells trap and cannibalize swarming neutrophils for metabolic independence

Project description:Neutrophils are activated and attracted to sites of anaphylaxis by degranulating tissue resident mast cells. After they facilitate inflammation and an anti-microbial immune response. However, the dynamics of neutrophils and direct interactions with mast cells are poorly investigated yet. By approaching 2-photon intravital microscopy and live cell imaging, we show that degranulating mast cells induce neutrophil swarming by releasing leukotriene B4 (LTB4). Attracted neutrophils interact with mast cells and surprisingly penetrate inside mast cells where they are stably trapped inside mast cell granules. We call this novel form of cell-in-cell structure “Mast Cell Intracellular Trap” (MIT). Trapped neutrophils and mast cells are both viable in the first 12 hours after MIT formation. However, neutrophils start to dye after 12hrs and translatome analysis of mast cells revealed improved mast cell metabolism and recovery. Therefore, neutrophils allow a faster and more efficient mast cell re-stimulation. Furthermore, mast cells get more resistant to extracellular nutrient limitations. Thus, beside their inflammatory role in anaphylaxis, neutrophils support mast cell recovery by forming a cell in cell structure. This might affect chronic inflammation and recurrent infections.

2024-06-07 | GSE168801 | GEO

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