Plasma miR-1 is downregulated in allergic rhinitis and alleviates IL-13-induced nasal epithelial inflammation via...

Allergic rhinitis (AR), a common chronic inflammatory disorder of the upper airway, currently lacks reliable non-invasive molecular biomarkers for dynamic disease monitoring and therapeutic guidance. This study aimed to evaluate the diagnostic value of plasma miR 1 in AR and to investigate its role in nasal epithelial inflammation and oxidative stress, along with the underlying molecular mechanism.

Plasma miR 1 was quantified by RT qPCR in 118 AR patients and 100 healthy controls, followed by correlation analysis with disease severity indices. An IL 13-stimulated human nasal epithelial cell (HNEpC) model was employed to examine viability, apoptosis, pro-inflammatory cytokines (IL 6, IL 8), and oxidative stress markers (MDA, GSH) following miR 1 overexpression or knockdown. Bioinformatic screening and dual-luciferase reporter assays were utilized to identify and validate BDNF as a direct miR 1 target. Rescue experiments were performed through co-transfection of miR 1 mimic with BDNF overexpression vector.

Plasma miR 1 was significantly lower in AR patients and negatively correlated with TNSS and RQLQ scores, yielding an AUC of 0.864 for discriminating AR from controls. In IL 13 treated HNEpC, miR 1 overexpression enhanced cell viability, reduced apoptosis, decreased IL 6 and IL 8 secretion, and ameliorated oxidative stress (lowered MDA, elevated GSH). BDNF was confirmed as a direct target of miR 1. BDNF overexpression partially reversed the protective effects of miR 1 upregulation.

Plasma miR 1 is downregulated in AR and correlates with disease severity, suggesting its potential as a non invasive diagnostic biomarker. Experimental evidence indicates that miR 1 may alleviate IL 13 induced inflammation and oxidative stress in HNEpC through direct targeting of BDNF.