Quercetin alleviates Der p 2-induced inflammatory response in airway epithelial cells by inhibiting mitochondrial overactivation

Objective To investigate the effects of the house dust mite allergen Der p 2 on mitochondrial function and inflammatory response in human bronchial epithelial cells (BEAS-2B) and to elucidate the interventional role of quercetin.Methods Using BEAS-2B cells as the model, different concentrations of Der p 2 (0, 10, 20, 30 μg/mL) and quercetin (0, 5, 10, 20, 30, 40 μM) were treated alone or in combination. Cell viability was assessed using the CCK-8 method, the mRNA expression levels of epithelial-derived alarmins (TSLP, IL-33, IL-25) and pro-inflammatory cytokines (IL-4, IL-6, IL-8) were detected by qRT-PCR, the intracellular ATP levels were measured using a bioluminescence method, and mitochondrial membrane potential was detected by the TMRE fluorescent probe.Results Der p 2 significantly reduced BEAS-2B cell viability in a dose-dependent manner (P = 0.000 9), while quercetin alone had no significant effect. However, quercetin dose-dependently reversed the reduction in cell viability induced by Der p 2 (P < 0.000 1). Der p 2 significantly upregulated the mRNA expression of TSLP, IL-33, IL-25, IL-4, IL-6, and IL-8 in BEAS-2B cells (all P < 0.05). Quercetin inhibited the expression of these factors (all P < 0.001), except for IL-4. Der p 2 exposure induced alterations in mitochondrial function in BEAS-2B cells: ATP production and mitochondrial membrane potential were significantly increased at 12 h (both P < 0.001), followed by a gradual decline. Quercetin significantly inhibited these effects (both P < 0.000 1).Conclusion Der p 2 mediates airway epithelial cell inflammatory response and reduced cell viability by inducing early mitochondrial hyperfunction and subsequent metabolic exhaustion. Quercetin alleviates Der p 2-induced epithelial cell damage and inflammation by modulating mitochondrial energy metabolism. This study provides new experimental evidence for targeting mitochondrial metabolism in the intervention of allergic asthma.