Contribution of small airway inflammation to the development of COPD

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Keywords: Chronic obstructive pulmonary disease; FeNO200; Peripheral airways; Small airway inflammation.