Abstract:

Objective To study the distribution and significance of CD1a and CD83 positive dendritic cells (DCs) in lung tissue of chronic obstructive pulmonary disease (COPD) mice. Methods Twenty C57BL/6 mice were randomly divided into the air control group and the smoked COPD group (n=10 for each group). COPD mouse model was established using cigarette smoking method. Mice were executed within 24 h after the last cigarette smoking, and right lower lung was collected. Body mass changes and lung histopathological changes of mice were observed in two groups. Mean linear intercept (MLI) was measured, and expression levels of CD1a⁺ and CD83⁺ DCs in lung tissue were detected by immunohistochemistry. Results The body mass of mice at 7, 14, 21 and 28 d after modeling was lower in the smoked COPD group than that in the air control group (P<0.05). HE staining showed that the normal alveolar structure of lung tissue of mice in the smoked group was disrupted, with multiple alveoli fused with each other to form a larger alveolar lumen, a large number of inflammatory cells infiltrated in alveolar intervals, and walls of the alveoli were thickened. COPD modeling was successful. Compared with the air control group, MLI values (μm) increased in the smoked COPD group (28.30±3.47 vs. 50.40±3.60), and the number of CD1a⁺ DCs ( per field of view) in lung tissue increased (9.58±2.18 vs. 17.08±3.67), while the number of CD83⁺ DCs (per field of view) decreased (19.78±4.95 vs. 8.02±3.30) (all P<0.05). Conclusion The number of CD1a⁺ DCs in lung tissue is increased and the number of CD83⁺ DCs in lung tissue is decreased in the smoked COPD group of mice, and cigarette smoking may have impaired DC maturation.

Key words: pulmonary disease, chronic obstructive, dendritic cells, smoking, CD1a, CD83