Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Institute of Respiratory Diseases, Soochow University, Suzhou, 215006, China.
BMC Pulm Med. 2024 Mar 20;24(1):144. doi: 10.1186/s12890-024-02962-6.
The causality of the relationship between bronchiectasis and chronic obstructive pulmonary disease (COPD) remains unclear. This study aims to investigate the potential causal relationship between them, with a specific focus on the role of airway inflammation, infections, smoking as the mediators in the development of COPD.
We conducted a two-sample Mendelian randomization (MR) analysis to assess: (1) the causal impact of bronchiectasis on COPD, sex, smoking status, infections, eosinophil and neutrophil counts, as well as the causal impact of COPD on bronchiectasis; (2) the causal effect of smoking status, infections and neutrophil counts on COPD; and (3) the extent to which the smoking status, infections and neutrophil counts might mediate any influence of bronchiectasis on the development of COPD.
COPD was associated with a higher risk of bronchiectasis (OR 1.28 [95% CI 1.05, 1.56]). Bronchiectasis was associated with a higher risk of COPD (OR 1.08 [95% CI 1.04, 1.13]), higher levels of neutrophil (OR 1.01 [95% CI 1.00, 1.01]), higher risk of respiratory infections (OR 1.04 [95% CI 1.02, 1.06]) and lower risk of smoking. The causal associations of higher neutrophil cells, respiratory infections and smoking with higher COPD risk remained after performing sensitivity analyses that considered different models of horizontal pleiotropy, with OR 1.17, 1.69 and 95.13, respectively. The bronchiectasis-COPD effect was 0.99, 0.85 and 122.79 with genetic adjustment for neutrophils, respiratory infections and smoking.
COPD and bronchiectasis are mutually causal. And increased neutrophil cell count and respiratory infections appears to mediate much of the effect of bronchiectasis on COPD.
支气管扩张症和慢性阻塞性肺疾病（COPD）之间的因果关系尚不清楚。本研究旨在探讨它们之间潜在的因果关系，特别关注气道炎症、感染、吸烟作为 COPD 发展的中介在其中的作用。
我们进行了两样本孟德尔随机化（MR）分析，以评估：（1）支气管扩张症对 COPD、性别、吸烟状况、感染、嗜酸性粒细胞和中性粒细胞计数的因果影响，以及 COPD 对支气管扩张症的因果影响；（2）吸烟状况、感染和中性粒细胞计数对 COPD 的因果影响；（3）吸烟状况、感染和中性粒细胞计数可能在多大程度上介导支气管扩张症对 COPD 发展的影响。
COPD 与支气管扩张症的风险增加相关（OR 1.28 [95% CI 1.05, 1.56]）。支气管扩张症与 COPD 的风险增加相关（OR 1.08 [95% CI 1.04, 1.13]），中性粒细胞水平更高（OR 1.01 [95% CI 1.00, 1.01]），呼吸道感染风险更高（OR 1.04 [95% CI 1.02, 1.06]），吸烟风险更低。在考虑不同水平的混杂偏倚模型后，进行敏感性分析，中性粒细胞、呼吸道感染和吸烟与 COPD 风险增加的因果关系仍然存在，OR 分别为 1.17、1.69 和 95.13。在对中性粒细胞、呼吸道感染和吸烟进行遗传调整后，支气管扩张症-COPD 的影响分别为 0.99、0.85 和 122.79。
COPD 和支气管扩张症是相互因果的。中性粒细胞计数增加和呼吸道感染似乎介导了支气管扩张症对 COPD 的大部分影响。
