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Integrative transcriptomic analysis in human and mouse models of anaphylaxis identifies upregulation of cell movement, migration and neuroinflammatory signalling pathway

ABSTRACT: 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.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE215184 | GEO | 2022/11/21

REPOSITORIES: GEO

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Genomic responses in blood during acute human anaphylaxis

Project description:Gene expression was profiled in peripheral blood samples collected over three time points from patients during acute anaphylaxis and from healthy controls. Patients presented to the Emergency Department (ED) at Royal Perth Hospital with acute, moderately severe anaphylaxis. Samples were collected at ED arrival (T0), 1 hour later (T1), and 3 hours post arrival (T2). The study design consisted of 12 subjects, 3 time points, and 2 clinical states (acute anaphylaxis, healthy controls).

2014-07-02 | E-GEOD-47655 | biostudies-arrayexpress

Genomic responses in blood during acute human anaphylaxis

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Origins and diversity of pan-isotype human bone marrow plasma cells

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2024-05-01 | GSE262896 | GEO

sncRNA in sera from childen with food anaphylaxis and adults with drug anaphylaxis

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2023-10-19 | GSE245653 | GEO

Gene expression patterns in blood during human anaphylaxis, trauma, and sepsis

Project description:Gene expression was profiled in peripheral blood samples collected from patients during anaphylaxis, trauma, or sepsis, and from healthy controls. Patients were recruited from three Australian emergency departments (ED) between March 2011 and June 2013. Samples were collected at ED arrival (T0), 1 hour later (T1), and 3 hours post arrival (T2).

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CD23+IgG1+ memory B cells are poised to switch to pathogenic IgE production in food allergy

Project description:Food allergy is caused by allergen-specific IgE but little is known about the B cell memory of persistent responses. Here we describe in pediatric peanut allergy a population of CD23+IgG1 memory B cells that contains peanut-specific clones and generates IgE plasma cells on activation. Through single cell transcriptomics and B cell receptor (BCR) sequencing, we characterized FCER2/CD23+ IgG1 memory B cells co-expressing IL4R, IL13RA1, IGHE and carrying highly mutated BCRs. Further we found that peanut allergen (Ara h 2)-specific B cells were mostly IgG1 memory cells, carried highly mutated BCRs compared to diphtheria toxin-specific B cells, and expressed FCER2 and germlin IGHE. Our findings suggest that CD23+IgG1+ memory B cells transcribing IGHE are a unique memory population containing precursors for pathogenic IgE in food allergy.

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2015-09-11 | E-GEOD-72921 | biostudies-arrayexpress

Characterization of anaphylaxis reveals different metabolic changes depending on severity and triggers - MS (part-II)

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

Characterization of anaphylaxis reveals different metabolic changes depending on severity and triggers - NMR (part-I)

2021-01-18 | ST001655 | MetabolomicsWorkbench

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