Kantar Ahmad, Song Woo-Jung, Bush Andrew, Chatziparasidis Grigorios
Paediatric Asthma and Cough Centre, Instituti Ospedalieri Bergamaschi, Bergamo, Italy.
Vita-Salute San Raffaele University, Milan, Italy.
ERJ Open Res. 2024 Dec 2;10(6). doi: 10.1183/23120541.00330-2024. eCollection 2024 Nov.
Non-cystic fibrosis bronchiectasis (NCFBE) belongs to the spectrum of chronic suppurative lung diseases and is characterised by persistent wet/sputum-productive cough and airway dilatation. Morphological and structural changes in the airways lead to changes in airflow, impair breathing-induced mucus transport and sliding, and reduce the shear forces of cough. Moreover, mucus hyperviscosity contributes to compromised ciliary activity and the pathogenesis of the disease. This mini-review highlights the role of cough in NCFBE, especially with respect to mucus clearance. Cough is the principal backup mechanism when mucus clearance is impaired due to either reduced function of cilia- and breathing-induced mucus transport, or abnormal mucus, or both. The efficiency of cough in overcoming the cohesive and adhesive properties of mucus is determined by both the forces applied to mucus by airflow and the mucus-airway surface properties. In NCFBE, mucus hyperviscosity contributes to impaired mucus clearance and determines disease pathogenesis; therefore, it may be a therapeutic target. The primary objectives of physiotherapy regimens in NCFBE are mucus hydration and the establishment of an optimal expiratory airflow velocity, which exerts shearing forces on the mucus located on the airway surface. Modifying the rheological properties of mucus and enhancing its transport whenever possible (by breathing manoeuvres, ciliary activity and cough) represent prime goals in preventing disease progression and, indeed reversing, bronchiectasis in the early stages of the disease, as well as preventing pulmonary exacerbations.
非囊性纤维化支气管扩张症(NCFBE)属于慢性化脓性肺部疾病范畴,其特征为持续的湿性/咳痰性咳嗽和气道扩张。气道的形态和结构变化导致气流改变,损害呼吸诱导的黏液转运和滑动,并降低咳嗽的剪切力。此外,黏液高黏滞性会导致纤毛活动受损和疾病的发病机制。本综述强调了咳嗽在NCFBE中的作用,特别是在黏液清除方面。当由于纤毛功能减退和呼吸诱导的黏液转运功能降低、黏液异常或两者兼而有之导致黏液清除受损时,咳嗽是主要的备用机制。咳嗽克服黏液黏聚性和黏附性的效率取决于气流对黏液施加的力以及黏液-气道表面特性。在NCFBE中,黏液高黏滞性导致黏液清除受损并决定疾病发病机制;因此,它可能是一个治疗靶点。NCFBE物理治疗方案的主要目标是使黏液水化并建立最佳呼气气流速度,该速度会对位于气道表面的黏液施加剪切力。改变黏液的流变学特性并尽可能增强其转运(通过呼吸动作、纤毛活动和咳嗽)是预防疾病进展以及在疾病早期逆转支气管扩张并预防肺部加重的主要目标。