Ontology highlight
ABSTRACT:
PROVIDER: PRJNA937049 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23651800_1.fastq.gz | Fastqsanger.gz | |||
| SRR23651800_2.fastq.gz | Fastqsanger.gz | |||
| SRR23651801_1.fastq.gz | Fastqsanger.gz | |||
| SRR23651801_2.fastq.gz | Fastqsanger.gz | |||
| SRR23651802_1.fastq.gz | Fastqsanger.gz |
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Project description:Epigenetic changes in food induced anaphylaxis animal model after immunotherapy.
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Project description:The underlying mechanisms of IgE-mediated anaphylaxis remain poorly understood. Furthermore, it remains to be determined to what extent findings from animal/mouse models reflects the pathophysiological mechanism in human. Therefore, to better characterize the mechanisms leading to potentially lethal events, analysis of global transcriptional changes (RNA-sequencing) in peripheral blood human samples in patients with anaphylaxis presenting at the emergency department and in patients with anaphylaxis during double-blind placebo-controlled food challenges (DBPCFC) to peanut, was performed. Mouse samples with different severity of IgE-mediated food-induced anaphylaxis were also included in RNA-sequencing analyses.
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Project description:Food-specific IgE triggers life-threatening anaphylaxis; however, some people with food-specific IgE are asymptomatic upon allergen consumption. Using murine food allergy models, we discovered an unexpected pathway regulating the ability of food allergens to trigger anaphylaxis. C57BL/6 mice are uniquely resistant to anaphylaxis when challenged orally; we show that goblet cells transport less food allergens relative to anaphylaxis-susceptible strains, even prior to allergic sensitization. In a forward genetic screen, oral anaphylaxis resistance correlated with Dipeptidase1 (Dpep1) allelic variants. DPEP1 is expressed in intestinal epithelium and catabolizes leukotriene D4 (LTD4). Blocking DPEP1 with cilastatin, genetically deleting Dpep1, or oral administration of LTD4 enhanced allergen transport in resistant mice. Conversely, pre-treatment of susceptible mice with a leukotriene synthesis inhibitor, zileuton, abrogated allergen absorption from the gut and subsequent oral anaphylaxis. Inhibiting leukotrienes may be a novel treatment for food allergy.
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Project description:Food-specific IgE triggers life-threatening anaphylaxis; however, some people with food-specific IgE are asymptomatic upon allergen consumption. Using murine food allergy models, we discovered an unexpected pathway regulating the ability of food allergens to trigger anaphylaxis. C57BL/6 mice are uniquely resistant to anaphylaxis when challenged orally; we show that their gut barrier was impermeable to food allergens relative to anaphylaxis-susceptible strains, even prior to allergic sensitization. In a forward genetic screen, oral anaphylaxis resistance correlated with Dipeptidase1 (Dpep1) allelic variants. DPEP1 is expressed in intestinal epithelium and catabolizes leukotriene D4. Blocking DPEP1 with cilastatin enhanced allergen absorption in resistant mice. Conversely, pre-treatment of susceptible mice with a leukotriene synthesis inhibitor, zileuton, abrogated allergen absorption and subsequent oral anaphylaxis. Inhibiting leukotrienes may be a novel treatment for food allergy.
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Project description:Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin (IL)-9. However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9 and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy.
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Project description:Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin (IL)-9. However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9 and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy. dUTP mRNA-Seq profiles of indicated hematopoietic cell lineages were generated on Illumina HiSeq2500. Hematopoietic cells were isolated from Balb/C mice that developed food allergy and bone marrow-derived mast cells were generated from naïve Balb/C mice
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Project description:Tolerance to dietary antigens is critical to avoid deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens is poorly understood. Here we demonstrate that the goblet cell-derived resistin-like molecule beta (RELMb) is a critical regulator of oral tolerance. We find that RELMb is abundant in serum in both food allergic patients and mouse models of FA. Deletion of RELMβ protects mice from FA, development of food antigen specific IgE and anaphylaxis. RELMb disrupts food tolerance through modulation of the gut microbiome by suppressing gut Lactobacilli. Tolerance is maintained via local production of indole derivatives driving FA protective RORgt+ regulatory T (Treg) cells via activation of the aryl hydrocarbon receptor (AhR). RELMb antagonism in the peri-weaning period restored oral tolerance and protected genetically prone offspring from developing FA later in life. Together, our data identify RELMb as mediating both a novel gut immune-epithelial circuit regulating tolerance to food antigens, a new mode of innate control of antigen specific adaptive immunity via microbiome editing and targetable candidates in this circuit for prevention and treatment of FA.
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