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Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

ABSTRACT: Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

PROVIDER: PRJNA1247394 | ENA |

REPOSITORIES: ENA

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Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

Project description:Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

| PRJNA1247403 | ENA

Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

Project description:Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

| PRJNA1245255 | ENA

Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

Project description:Anaphylaxis is a life-threatening complication of allergen exposure. While mechanisms governing anaphylaxis after intravenous injection have been defined in mice, these models neglect mucosal exposure that accompanies food ingestion. We investigated the role of mast cell populations within the intestine of mice in response to antigens delivered orally. Oral anaphylaxis required IgE-FcεR1 signaling, and profiling of intestinal mast cells revealed a rapidly developing population shaped by epithelial cues. Intestinal mast cells were largely epithelium-resident and displayed divergent transcriptomes and effector functions from connective tissue mast cells found throughout the body. Histamine synthesis was diminished and leukotriene generation enhanced. Mice genetically deficient in cysteinyl leukotriene synthesis, or those treated with aLOX5 antagonist, Zileuton, were protected from oral anaphylaxis whereas that elicited by intravenous injection was unaltered.

2025-08-07 | GSE293904 | GEO

Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

2025-08-07 | GSE293561 | GEO

Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-07 | GSE293906 | GEO

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

2013-03-09 | GSE44980 | GEO

Transcription profiling of mouse hematopoietic stem cell, mast cell precursor and mature mast cell

Project description:We are interested in comparing expression patterns of hematopoletic stem cells, mast cell precursors and mature mast cells. Our group recently reported that murine mast cells express CD34, Sca-1 and c-kit. Microarray analysis may uncover other novel surface antigens useful in separating mast cells from stem cells. Experiment Overall Design: this experiment include 2 samples and 12 replicates

2008-06-12 | E-GEOD-3776 | biostudies-arrayexpress

Comparison of Hematopoietic Stem Cell, Mast Cell Precursor and Mature Mast Cell Gene Expression

2005-12-09 | GSE3776 | GEO

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

Crosstalk between Regnase-1 and -3 shapes mast cell survival and cytokine expression

Project description:Dysregulation of mast cell activation can lead to allergic and anaphylactic reactions. Post-transcriptional regulation of immune-related transcripts by RNA-binding proteins (RBPs) is critical in controlling immune cell responses, including mast cell functionality. The Regnase family of RBPs plays a central role in regulating gene expression and controlling immune responses in both lymphoid and myeloid cells. However, what is the functional role of Regnase proteins in mast cells remains to be understood. Using different approaches of Regnase proteins depletion and deletion as well as overexpression by mRNA delivery, we found that Regnase-1 is a powerful negative regulator of mast cell proliferation, survival and ability to produce inflammatory cytokines. On the other hand, Regnase-3 was essential to modulate Regnase-1 expression in mast cells by direct targeting of the 3’-untranslated region of Regnase-1, leading to the destabilization of the Zc3h12a mRNA. Regnase-1 deletion had widespread effect on mast proliferation and survival even in the absence of stimulation and was at least in part linked to specific nuclear functions of Regnase-1 in modulating the ability of mast cells to withstand DNA damage. Overall, we describe the importance of Regnase proteins in modulating mast cell homeostatic and inflammatory responses and we describe the impact of Regnase-1 in the maintenance of genome stability.

2024-05-31 | GSE240035 | GEO

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