House dust mite-induced autophagy dysregulation and apoptosis in bronchial epithelial injury in asthma.

INTRODUCTION: Airway epithelial injury is a central feature of asthma and contributes to persistent airway inflammation, mucus overproduction, and airway remodeling. House dust mite (HDM) is a major aeroallergen associated with allergic asthma, yet the intracellular stress responses underlying HDM-induced epithelial damage remain incompletely understood. Here, we investigated changes in the autophagic process and apoptotic signaling during HDM-induced airway injury using both in vivo and in vitro models. METHODS: Wild-type BALB/c mice were exposed to HDM by intranasal administration, and airway pathology was evaluated using hematoxylin and eosin staining (H&E) and periodic acid-Schiff (PAS) staining. BEAS-2B bronchial epithelial cells were treated with HDM in vitro, followed by transmission electron microscopy (TEM), immunofluorescence (IF) staining, and Western blot to assess ultrastructural changes and the expression of autophagy- and apoptosis-related proteins. RESULTS: HDM exposure induced asthma-like airway pathology in mice, characterized by peribronchial inflammatory infiltration and increased mucus production. In bronchial epithelial cells, HDM caused mitochondrial ultrastructural injury and autophagosome accumulation, suggesting disruption of epithelial intracellular homeostasis. Further analyses showed increases in LC3-related signals and p62 levels, suggesting dysregulated autophagic processing. These autophagy-related alterations were accompanied by activation of apoptotic signaling. DISCUSSION: Taken together, our findings indicate that HDM-induced airway epithelial injury is accompanied by autophagy dysregulation and activation of apoptotic signaling. These results provide insight into epithelial stress responses involved in allergic airway inflammation and highlight autophagic dysregulation and apoptosis as cellular events associated with HDM-related bronchial epithelial damage.