Contribution of small airway inflammation to the development of COPD

Little attention has been paid to the pathophysiological changes in the natural history of chronic obstructive pulmonary disease (COPD). The destructions of the small airways were visualized on thoracic micro-computed tomography scan. We investigated whether small airway inflammation (SAI) was the risk for the development of COPD.

A total of 1062 patients were enrolled and analyzed in the study. The partitioned airway inflammation was determined by exhaled nitric oxide (NO) of FnNO, FeNO₅₀, FeNO₂₀₀, and calculated CaNO_dual. Both FeNO₂₀₀ and CaNO_dual were compared to detect the promising predictor for peripheral airway/alveolar inflammation in COPD. The correlation between exhaled NO and white cell classification was evaluated to determine the inflammation type during the development of COPD.

Exhaled NO levels (FnNO, FeNO₅₀, FeNO₂₀₀, and CaNO_dual) were the highest in the COPD group compared with all other groups. Furthermore, compared with controls, exhaled NO levels (FeNO₅₀, FeNO₂₀₀, and CaNO_dual) were also significantly higher in the emphysema, chronic bronchitis, and smoking groups. FeNO₂₀₀ was found to be a promising predictor for peripheral airway/alveolar inflammation (area under the curve [AUC] of the receiver operating characteristic [ROC] curve, area under the curve [AUC] = 0.841) compared with CaNO_dual (AUC ROC = 0.707) in COPD. FeNO₂₀₀ was the main risk factor (adjusted odds ratio, 2.191; 95% CI, 1.797-2.671; p = 0.002) for the development of COPD. The blood eosinophil and basophil levels were correlated with FeNO₅₀ and FeNO₂₀₀.

The complete airway inflammations were shown in COPD, whereas SAI was the main risk factor for the development of COPD, which might relate to eosinophil and basophil levels.