Airway inflammation drives both the development of bronchiectasis and results in the dominant clinical features. Many aetiologies of bronchiectasis, including previous infection, COPD, rheumatoid arthritis, allergic bronchopulmonary aspergillosis and toxic exposures, cause airway inflammation that damages the bronchial wall, which then allows chronic infection to be established. When bronchiectasis is caused by defects in airway immunity, although the disease maybe initiated by persistent bacterial bronchial infection, the inflammatory response to these bacteria then promotes worsening bronchiectasis through further damage to the bronchi. Once bronchiectasis is established, the degree of airway inflammation is closely correlated to the bacterial load in both stable disease and exacerbations [1–5].

气道炎症促进支气管扩张的发展并导致主要的临床特征。支气管扩张的许多病因，包括既往感染、慢性阻塞性肺病、类风湿性关节炎、过敏性支气管肺曲霉病和有毒物质暴露，都会引起气道炎症，损害支气管壁，从而形成慢性感染。当支气管扩张是由气道免疫缺陷引起时，尽管该疾病可能是由持续的细菌性支气管感染引发的，但对这些细菌的炎症反应会通过进一步损害支气管而促进支气管扩张恶化。一旦支气管扩张形成，气道炎症程度与疾病稳定期和恶化期的细菌载量密切相关[1-5]。