凋亡和凋亡细胞清除在慢性阻塞性肺疾病发病机制的地位

Status of apopotosis and efferocytosis in chronic obstructive pulmonary disease

吸烟是导致慢性阻塞性肺疾病（CODP）气道炎症的主要原因，但戒烟并不能减轻气道炎症，且炎症持续存在，疾病进行性发展和恶化。肺内凋亡细胞清除（胞葬作用：Efferocytosis）缺失可能与其有关，这种现象在COPD发生发展起重要作用。专职和非专职吞噬细胞识别凋亡细胞的过程具有抗炎、抗免疫和抗蛋白水解的作用，并诱导维持肺泡细胞生长因子产生和分泌，其功能缺失将导致凋亡细胞清除降低。一旦凋亡细胞识别缺失，这些作用也随之紊乱，这将对COPD发病机制起重要的作用。凋亡细胞清除缺失这一关键问题如何被发现和如何被控制？至今未有答案。

Cigarette smoking is a main trigger for the development of COPD,smoking cessation can not reduce bronichial inflammation,and the inflammation is continuous,and progressive and worse of COPD, which is associated with ineffective efferocytosis （defectiove clearance of apoptotic cell）, the phenomenon serves important role in pathogenesis of COPD. recognition of apoptotic cells directly induces professional phagocytes and nonprofessional phagocytes （fiboblasts, epithelial cell, and endothelial cell） to produce antinflammatory,antimmunogenic,and antiproteolytic effects,while induces growth maintenance factors for alveolar cells, impairment in these responses may result in ineffective efferocytosis, if disrupted in COPD, each of which could contribute to its pathogenesis. One of the key questions, so far unanswered, raised by inneffective efferocytosis is how many of these defects can be blocked or even reversed.