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ABSTRACT:
PROVIDER: PRJNA937049 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Epigenetic changes in food induced anaphylaxis animal model after immunotherapy.
| PRJNA905809 | ENA
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.
2022-11-21 | GSE215184 | GEO
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.
2015-09-11 | GSE72921 | GEO
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
2015-09-11 | E-GEOD-72921 | biostudies-arrayexpress
Project description:Transcriptional profiling of dendritic cells in a mouse model of food-antigen induced anaphylaxis using RNA-Seq
| PRJNA507608 | ENA
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.
2022-12-27 | GSE221462 | GEO
Project description:Background: Despite its increasing incidence, the underlying molecular processes of anaphylaxis remain unclear and there are not known biomarkers for appropriate diagnosis. The mechanism associated to the reactions still needs to be clarified in humans. The rapid onset and potentially fatal outcome in the absence of managed treatment, prevent its study and prompt obvious technical and ethical implications. Methods: Twenty episodes of anaphylaxis were analyzed. Sera was collected at different times: during the acute phase (T1), the recovery phase (T2) and around 2-3 months after the anaphylactic reaction (T0). The analysis included untargeted metabolomics combining liquid chromatography coupled to mass spectrometry (LC-MS) and proton-nuclear magnetic resonance (1H-NMR). Reactions were classified according to the trigger (food and/or drug) and severity (moderate and severe). Results: “Food T1 vs T2” and “moderate T1 vs T2” anaphylaxis comparisons showed clear metabolic patterns during the onset of an anaphylactic reaction, which differed from those induced by drugs, food+drug or severe anaphylaxis “T1 vs T2”. Moreover, the model of food anaphylaxis was able to distinguish the well-characterized IgE (beta-lactam) from non-IgE- mediated anaphylaxis (NSAIDs), suggesting a differential metabolic pathway associated with the mechanism of action. Moreover, metabolic differences between “moderate vs severe” at T1 and T0 were studied. Among the metabolites, glucose, lipids, cortisol, betaine and oleamide were observed altered. Conclusions: The results of the study provide the first evidence that different anaphylactic triggers, induce differential metabolic changes. Besides, the basal status might identify high risk patients, thus opening new ways to understand, diagnose and treat anaphylaxis.
2021-01-15 | ST001656 | MetabolomicsWorkbench
Project description:Background: Despite its increasing incidence, the underlying molecular processes of anaphylaxis remain unclear and there are not known biomarkers for appropriate diagnosis. The mechanism associated to the reactions still needs to be clarified in humans. The rapid onset and potentially fatal outcome in the absence of managed treatment, prevent its study and prompt obvious technical and ethical implications. Methods: Twenty episodes of anaphylaxis were analyzed. Sera was collected at different times: during the acute phase (T1), the recovery phase (T2) and around 2-3 months after the anaphylactic reaction (T0). The analysis included untargeted metabolomics combining liquid chromatography coupled to mass spectrometry (LC-MS) and proton-nuclear magnetic resonance (1H-NMR). Reactions were classified according to the trigger (food and/or drug) and severity (moderate and severe). Results: “Food T1 vs T2” and “moderate T1 vs T2” anaphylaxis comparisons showed clear metabolic patterns during the onset of an anaphylactic reaction, which differed from those induced by drugs, food+drug or severe anaphylaxis “T1 vs T2”. Moreover, the model of food anaphylaxis was able to distinguish the well-characterized IgE (beta-lactam) from non-IgE- mediated anaphylaxis (NSAIDs), suggesting a differential metabolic pathway associated with the mechanism of action. Moreover, metabolic differences between “moderate vs severe” at T1 and T0 were studied. Among the metabolites, glucose, lipids, cortisol, betaine and oleamide were observed altered. Conclusions: The results of the study provide the first evidence that different anaphylactic triggers, induce differential metabolic changes. Besides, the basal status might identify high risk patients, thus opening new ways to understand, diagnose and treat anaphylaxis.
2021-01-18 | ST001655 | MetabolomicsWorkbench
Project description:Regulatory and Effector T cells in Oral Immunotherapy for Food Allergy
| PRJNA565273 | ENA
Project description:Regulatory and Effector T cells in Oral Immunotherapy for Food Allergy
| PRJNA565274 | ENA