ArticleFrontiers in allergy2026
Exploration of miRNAs promoting eosinophilia and type 2 immunity.
Article in Frontiers in allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: MicroRNAs (miRNAs) are evolutionary conserved, small non-coding RNAs that regulate gene expression and modulate cellular responses. In this study, we profiled miRNAs regulated by interleukin-33 (IL-33), a key inflammatory mediator of allergic responses and type 2 immunity that promotes bone marrow eosinophil development and subsequent airway recruitment. Method: C57BL/6 mice were exposed to recombinant IL-33 intranasally to induce airway eosinophilia. Cellular composition was determined by differential cell counts in bronchoalveolar lavage fluid and bone marrow. RNA profiling was performed using miRNA microarray, NanoString nCounter (miRNA and mRNA), qPCR (miRNA), and PrimeFlow-a method combining flow cytometry with single-cell miRNA detection. Result: IL-33 challenge induced bone marrow eosinophilopoiesis and a significant influx of eosinophils into the airways. IL-33 altered miRNA expression in the lungs, displaying a distinct profile compared to IL-33-responsive miRNAs in the bone marrow. miRNAs previously implicated in regulating eosinophil development (e.g., miR-223-3p and miR-21) and type 2 lymphocyte effector functions (e.g., miR-155-5p, miR-150-5p) were significantly altered. These changes were accompanied by gene expression alterations in mediators associated with eosinophil migration (e.g., Conclusion: We identify candidate miRNA programs involved in the progression of IL-33-dependent eosinophilic inflammation from bone marrow induction to lung recruitment.
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