Interactions Via α(2)β(1) Cell Integrin May Protect against the Progression of Airway Structural Changes in Asthma

Increased airway wall thickness and remodeling of bronchial mucosa are characteristic of asthma and may arise from altered integrin signaling on airway cells. Here, we analyzed the expression of β(1)-subfamily integrins on blood and airway cells (flow cytometry), inflammatory biomarkers in serum and bronchoalveolar lavage, reticular basement membrane (RBM) thickness and collagen deposits in the mucosa (histology), and airway geometry (CT-imaging) in 92 asthma patients (persistent airflow limitation subtype: n = 47) and 36 controls. Persistent airflow limitation was associated with type-2 inflammation, elevated soluble α(2) integrin chain, and changes in the bronchial wall geometry. Both subtypes of asthma showed thicker RBM than control, but collagen deposition and epithelial α(1) and α(2) integrins staining were similar. Type-I collagen accumulation and RBM thickness were inversely related to the epithelial expression of the α(2) integrin chain. Expression of α(2)β(1) integrin on T-cells and eosinophils was not altered in asthma. Collagen I deposits were, however, more abundant in patients with lower α(2)β(1) integrin on blood and airway CD8(+) T-cells. Thicker airway walls in CT were associated with lower α(2) integrin chain on blood CD4(+) T-cells and airway eosinophils. Our data suggest that α(2)β(1) integrin on inflammatory and epithelial cells may protect against airway remodeling advancement in asthma.