Neutrophil Fates in Bronchiectasis and Alpha-1 Antitrypsin Deficiency
Neutrophil Fates in Bronchiectasis and Alpha-1 Antitrypsin Deficiency
复制标题
DOI：
10.1513/annalsats.201512-805kv
复制
发表时间：
2016-04-01
影响因子：
8.3
通讯作者：
Solomon, George M.
中科院分区：
文献类型：
--
作者：
Russell, Derek W.;Gaggar, Amit;Solomon, George M.
中性粒细胞是环境与肺组织之间脆弱界面的强大细胞防御者。这种细胞的强大武器在健康状态下经过仔细校准，以最大限度地提高对抗病原体的有效性，同时最大限度地减少组织损伤并允许修复已发生的损伤。囊性纤维化、非囊性纤维化支气管扩张和 α-1 抗胰蛋白酶缺乏这三种相关的慢性气道疾病均表现出这种稳态系统的显着紊乱，从而导致各自的病理学。它们之间一个重要的共同特征是慢性炎症的解决效率低下，而慢性炎症是中性粒细胞驱动的肺损伤导致疾病进展的主要手段。根据免疫病理学检查这些疾病之间的共性和差异，可以提供丰富的信息，并可能有助于指导我们未来设计旨在调节中性粒细胞与肺部环境相互作用的治疗方法。
The neutrophil is a powerful cellular defender of the vulnerable interface between the environment and pulmonary tissues. This cell's potent weapons are carefully calibrated in the healthy state to maximize effectiveness in fighting pathogens while minimizing tissue damage and allowing for repair of what damage does occur. The three related chronic airway disorders of cystic fibrosis, non-cystic fibrosis bronchiectasis, and alpha-1 antitrypsin deficiency all demonstrate significant derangements of this homeostatic system that result in their respective pathologies. An important shared feature among them is the inefficient resolution of chronic inflammation that serves as a central means for neutrophil-driven lung damage resulting in disease progression. Examining the commonalities and divergences between these diseases in the light of their immunopathology is informative and may help guide us toward future therapeutics designed to modulate the neutrophil's interplay with the pulmonary environment.