miR-337-5p targets WNK1 to promote IL-13-induced nasal epithelial inflammation in allergic rhinitis

Introduction: Allergic rhinitis (AR) represents a prevalent chronic inflammatory disease affecting the nasal mucosa, yet effective diagnostic biomarkers and therapeutic targets remain elusive. This investigation sought to examine plasma miR-337-5p expression and its diagnostic utility in AR patients, additionally dissecting its role and molecular mechanism during IL-13-induced nasal epithelial inflammatory injury. Methods: RT-qPCR quantified plasma miR-337-5p in 100 AR patients versus 100 controls, with ROC curve analysis establishing diagnostic value. For in vitro experiments, IL-13 exposure generated a Th2-type inflammation model in HNEpC cells. Post-transfection with miR-337-5p mimic or inhibitor, assessments encompassed cell viability, apoptosis, inflammatory cytokines (IL-6, IL-8), plus oxidative stress markers (SOD, MDA). Bioinformatics predicted target genes, subsequently validated through dual-luciferase reporter assay. Rescue experiments further clarified WNK1 involvement. Results: AR patients exhibited significantly higher plasma miR-337-5p concentrations, which correlated positively with TNSS scores and eosinophil counts. The resulting ROC curve demonstrated an AUC of 0.840, reflecting good diagnostic value. Within IL-13-stimulated HNEpC cells, miR-337-5p overexpression worsened cell injury, apoptosis, inflammatory cytokine release, and oxidative stress, while miR-337-5p inhibition conferred protection. Bioinformatics, coupled with dual-luciferase reporter assay, identified WNK1 as a direct miR-337-5p target. WNK1 expression was reduced in AR patients and showed a negative correlation with miR-337-5p levels. WNK1 knockdown partially abrogated the protective impact of miR-337-5p inhibition. Conclusions: Increased plasma miR-337-5p holds potential as a diagnostic biomarker for AR. Through WNK1 targeting, miR-337-5p aggravates IL-13-induced nasal epithelial inflammatory injury, implicating its contribution to AR pathogenesis.