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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

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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

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