Supplementary Material for: MiR-132-3p Regulates Inflammatory Response by Targeting JAK1 in Childhood Allergic Rhinitis and Chronic Rhinosinusitis

Introduction: Chronic rhinosinusitis (CRS) is a common chronic inflammatory disease in children, often comorbid with allergic rhinitis (AR). The role of miR-132-3p with AR and CRS in children remains unclear. To evaluate the diagnostic value and regulatory mechanism of miR-132-3p for pediatric AR-complicated CRS with nasal polyposis (CRSwNP).
Methods: A total of 265 children were enrolled, including 90 AR cases and 175 AR-complicated CRSwNP cases. Serum miR-132-3p and JAK1 expression were detected by RT-qPCR. ROC curve, correlation, and multivariate logistic regression analyses were used to assess diagnostic value and clinical associations. House dust mite extract (HDM)-induced human nasal epithelial cells (HNEpCs) were used as the inflammation model. Cell transfection, ELISA, and dual-luciferase reporter assay were performed to verify the regulatory mechanism.
Results: Serum miR-132-3p was significantly downregulated in the CRS versus AR group, and miR-132-3p was lower in eosinophil CRSwNP (ECRSwNP) than non-eosinophilic CRS (NECRSwNP). In HNEpCs, HDM reduced miR-132-3p and elevated JAK1, IL-25, IL-33, and TSLP. miR-132-3p mimics inhibited the upregulation of these factors and directly targeted JAK1. JAK1 overexpression reversed the inhibitory effect of miR-132-3p.
Conclusions: miR-132-3p is significantly downregulated in the serum of children with AR-complicated CRSwNP, which can serve as a non-invasive diagnostic marker for differentiating NECRSwNP from ECRSwNP, and is associated with disease severity. It regulates HDM-mediated type 2 inflammation by targeting JAK1, participating in CRSwNP pathogenesis.