Role of miR-191-3p in HDM-induced airway epithelial inflammation by targeting CD247 in allergic asthma

Allergic asthma is a helper T cell-driven chronic airway inflammation. This study evaluated the clinical significance of miR-191-3p in allergic asthma and its role in regulating airway epithelial inflammation via CD247.

qRT-PCR was employed to determine miR-191-3p levels in 125 allergic asthma patients and 105 healthy controls. ROC curve assessed diagnostic value. Pearson and logistic regression analyzed clinical correlations and predictive factors. BEAS-2B cells were HDM-stimulated to establish an inflammation model. After miR-191-3p inhibitor transfection, inflammatory and oxidative stress were assessed. The miR-191-3p/CD247 interaction was predicted bioinformatically and confirmed by dual-luciferase assay. Rescue experiments validated the role of this axis in airway inflammation.

Serum miR-191-3p was significantly elevated in allergic asthma patients versus controls (AUC = 0.841), was positively correlated with total IgE and eosinophil counts, and was identified as an independent risk factor for asthma. In BEAS-2B cells, HDM stimulation upregulated miR-191-3p expression, increased inflammatory release, and induced oxidative stress imbalance, all of which were reversed by miR-191-3p inhibition. Mechanistically, CD247 was validated as a direct target of miR-191-3p. Rescue experiments showed that CD247 silencing partially abolished the anti-inflammatory effects of miR-191-3p inhibition.

miR-191-3p is significantly upregulated both in allergic asthma patients and in house dust mite-stimulated airway epithelial cells. These findings indicate that miR-191-3p may contribute to airway inflammation and oxidative stress through targeted regulation of CD247 expression.