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[慢性阻塞性肺疾病中的结构异常与炎症:聚焦于小气道]

[Structural abnormalities and inflammation in COPD: a focus on small airways].

作者信息

Burgel P-R, Bourdin A, Pilette C, Garcia G, Chanez P, Tillie-Leblond I

机构信息

Service de pneumologie, hôpital Cochin, AP-HP, université Paris Descartes, Paris, France.

出版信息

Rev Mal Respir. 2011 Jun;28(6):749-60. doi: 10.1016/j.rmr.2011.01.009. Epub 2011 May 25.

DOI:10.1016/j.rmr.2011.01.009
PMID:21742236
Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by poorly reversible airflow limitation associated with airway remodelling and inflammation of both large and small airways. The site of airflow obstruction in COPD is located in the small airways, justifying a focus on this compartment. The structural abnormalities that are found in bronchioles with a diameter less than 2mm are characterized by increased airway wall thickness with peribronchial fibrosis, and by luminal obstruction by mucous exudates. Destruction of alveolar walls, the hallmark of emphysema, may be related to protease-antiprotease imbalance, and to mechanisms involving apoptosis, senescence, and autoimmunity. Cigarette smoke inhalation triggers the recruitment of innate immune cells (neutrophils and macrophages) and putatively adaptive immunity mediated via T and B lymphocytes and lymphoid follicles in the small airways. These data suggest a potential role for therapies that can target remodelling and inflammation in the small airways of patients with COPD.

摘要

慢性阻塞性肺疾病(COPD)的特征是气流受限难以逆转,伴有气道重塑以及大小气道的炎症。COPD气流阻塞的部位位于小气道,这使得对该区域的关注具有合理性。在直径小于2mm的细支气管中发现的结构异常,其特征是气道壁厚度增加并伴有支气管周围纤维化,以及黏液渗出物导致的管腔阻塞。肺泡壁破坏是肺气肿的标志,可能与蛋白酶-抗蛋白酶失衡以及涉及细胞凋亡、衰老和自身免疫的机制有关。吸入香烟烟雾会引发固有免疫细胞(中性粒细胞和巨噬细胞)的募集,并可能通过T和B淋巴细胞以及小气道中的淋巴滤泡介导适应性免疫。这些数据表明,针对COPD患者小气道重塑和炎症的治疗方法可能具有潜在作用。

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