Association of MiR-27a-5p with chronic obstructivepulmonary disease and its role in human bronchial epithelialcell injury: A case-control and in vitro experimental study

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) lacks effective early diagnostic biomarkers, and the role of miR-27a-5p in COPD pathogenesis remains unclear. This study aimed to explore its inflammatory regulatory mechanism. METHODS: We enrolled COPD patients and healthy controls, measuring miR-27a-5p and inflammatory cytokines (TNF-α, IL-6, IL-1β) in serum and bronchoalveolar lavage fluid. Multivariate logistic regression and ROC curves were used to analyze disease association and diagnostic efficacy. A cigarette smoke extract-induced bronchial epithelial cell model was used with miRNA transfection and dual-luciferase assays to validate the target gene and mechanism. RESULTS: MiR-27a-5p was significantly upregulated in COPD patients (p<0.001), and its expression was associated with COPD alongside smoking status and pulmonary function (adjusted odds ratio, AOR=22.53; 95% CI: 12.31-41.30, p<0.001). It showed strong diagnostic efficacy (AUC=0.96; 95% CI: 0.92-0.99). In vitro, miR-27a-5p overexpression exacerbated inflammation, while inhibition alleviated it. Mechanistically, miR-27a-5p directly targeted ABL2 to regulate inflammatory cytokine release. CONCLUSIONS: MiR-27a-5p within our study was identified as a promising biomarker for COPD susceptibility and modulated airway inflammation via the miR-27a-5p-ABL2 axis.