Aubier M, Marthan R, Berger P, Chambellan A, Chanez P, Aguilaniu B, Brillet P-Y, Burgel P-R, Chaouat A, Devillier P, Escamilla R, Louis R, Mal H, Muir J-F, Pérez T, Similowski T, Wallaert B, Roche N
Inserm U 700, Service de Pneumologie A, Hôpital Bichat-Claude-Bernard, Groupement Hospitalier Universitaire Nord, Faculté de Médecine de Paris-Diderot, 46 Rue Henri-Huchard, 75018 Paris 7, France.
Rev Mal Respir. 2010 Dec;27(10):1254-66. doi: 10.1016/j.rmr.2010.10.004. Epub 2010 Nov 11.
The present study reviews the literature on inflammation and remodelling mechanisms in chronic obstructive pulmonary disease (COPD). The development of COPD is associated with chronic pulmonary inflammation. Immunity (innate or adaptive) plays a role in its onset and continuation. Airways inflammation alters bronchial structure/function relations: increased bronchial wall thickness, increased bronchial smooth muscle tone, seromucosal gland hypersecretion and loss of elastic structures. Circulating markers of pulmonary inflammation indicate its systemic dissemination. Oxidative stress plays a major role in the onset and persistence of tissue abnormalities. The determinants of extra- and intra-cellular redox control are only partially known. Susceptibility genes, antioxidant system insufficiency and reduced levels of anti-age molecules and of histone deacetylation are also involved. The molecular and cellular targets of inflammation and remodelling are numerous and complex. Currently, tools exist to limit inflammation in COPD but not to act on structural remodelling.
本研究回顾了关于慢性阻塞性肺疾病（COPD）炎症和重塑机制的文献。COPD的发展与慢性肺部炎症相关。免疫（先天性或适应性）在其发病和持续过程中起作用。气道炎症改变支气管结构/功能关系：支气管壁厚度增加、支气管平滑肌张力增加、浆液黏液腺分泌亢进以及弹性结构丧失。肺部炎症的循环标志物表明其全身扩散。氧化应激在组织异常的发生和持续中起主要作用。细胞内外氧化还原控制的决定因素仅部分为人所知。易感性基因、抗氧化系统不足以及抗老化分子和组蛋白去乙酰化水平降低也参与其中。炎症和重塑的分子和细胞靶点众多且复杂。目前，存在限制COPD炎症的工具，但尚无作用于结构重塑的工具。
