ArticleBMC immunology2026
Role of miR-191-3p in HDM-induced airway epithelial inflammation by targeting CD247 in allergic asthma.
Article in BMC immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAllergic 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.
methodsqRT-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.
resultsSerum 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.
conclusionsmiR-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.
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