MiR-132-3p Regulates Inflammatory Response by Targeting JAK1 in Childhood Allergic Rhinitis and Chronic...

Area of Science:

• Immunology
• Genetics
• Pediatrics

Background:

• Chronic rhinosinusitis (CRS) is a prevalent inflammatory condition in children, frequently co-occurring with allergic rhinitis (AR).
• The specific role of microRNA-132-3p (miR-132-3p) in pediatric AR and CRS remains largely undefined.
• Understanding miR-132-3p's function is crucial for diagnosing and managing pediatric AR-complicated CRS with nasal polyposis (CRSwNP).

Purpose of the Study:

• To evaluate the diagnostic utility of miR-132-3p in pediatric patients with AR-complicated CRSwNP.
• To elucidate the regulatory mechanism of miR-132-3p in the context of CRSwNP.
• To investigate the association between miR-132-3p levels and disease characteristics.

Main Methods:

• Serum samples from 265 children (90 AR, 175 AR-complicated CRSwNP) were analyzed for miR-132-3p and JAK1 expression using RT-qPCR.
• Diagnostic value was assessed via ROC curve, correlation, and logistic regression analyses.
• An in vitro model using house dust mite (HDM)-stimulated human nasal epithelial cells (HNEpCs) was employed to study miR-132-3p's regulatory role, involving cell transfection, ELISA, and dual-luciferase reporter assays.

Main Results:

• Serum miR-132-3p levels were significantly lower in children with CRS compared to those with AR.
• miR-132-3p expression was reduced in eosinophilic CRSwNP (ECRSwNP) compared to non-eosinophilic CRS (NECRSwNP).
• In HDM-induced HNEpCs, miR-132-3p downregulation correlated with increased JAK1, IL-25, IL-33, and TSLP; miR-132-3p mimics suppressed these factors and directly targeted JAK1, with JAK1 overexpression reversing these effects.

Conclusions:

• miR-132-3p is significantly downregulated in the serum of children with AR-complicated CRSwNP, offering potential as a non-invasive diagnostic biomarker.
• miR-132-3p can differentiate between NECRSwNP and ECRSwNP and correlates with disease severity.
• The study demonstrates that miR-132-3p regulates HDM-induced type 2 inflammation by targeting JAK1, thus playing a role in CRSwNP pathogenesis.