中性粒细胞胞外诱捕网在哮喘和慢性阻塞性肺疾病中的作用

2017/07/24

   摘要
   目的:哮喘和慢性阻塞性肺疾病(COPD)是具代表性的有较大疾病负担的慢性炎性气道疾病。本文综述了中性粒细胞胞外诱捕网(NETs)和慢性炎性气道疾病之间的关系。
   数据来源:截止到2017年1月1日,发表在PubMed, Ovid Medline, Embase 数据库,关键词是“哮喘”或“肺部疾病,慢性阻塞性”,“中性粒细胞”和“胞外诱捕网”的文章。
   研究选择:获取并评价文章以分析NETs在哮喘和COPD中的作用。
   结果:NETs由活化的中性粒细胞释放的DNA、组蛋白和颗粒蛋白构成。众多研究已经表明在哮喘和COPD患者气道中有大量的NETs。NETs可以吞噬并杀死入侵宿主的病原体。然而,已有研究证明NET形成的调控异常与哮喘和COPD的发生发展有关。在气道和肺组织中过多的NETs会通过诱导人类上皮细胞和内皮细胞的死亡造成不同程度的肺组织损伤,因而导致肺功能的损伤并加速疾病进展。
   结论:哮喘和COPD患者气道中存在过多的NETs聚集。尽管NETs在固有免疫系统抗感染的过程中发挥了必要的作用,但过多的NETs成分会造成哮喘和COPD患者的肺组织损伤并促进疾病进展。这些发现表明对NETs的管理可能是治疗哮喘和COPD的新方法,急需哮喘和慢阻肺患者中性粒细胞活化调节或NET功能直接阻断相关的机制研究、临床试验以及临床策略。
 
 
(复旦大学附属中山医院呼吸科 王晓岑摘译 杨冬审校)
(Chin Med J (Engl). 2017 Mar 20;130(6):730-736. doi: 10.4103/0366-6999.201608.)


 
 
 
Role of Neutrophil Extracellular Traps in Asthma and Chronic ObstructivePulmonary Disease.
 
Liu T, Wang FP, Wang G, et al
 
Abstract
OBJECTIVE: Asthma and chronic obstructive pulmonary disease (COPD) arerepresentative chronic inflammatory airway diseases responsible for a
considerable burden of disease. In this article, we reviewed the relationshipbetween neutrophil extracellular traps (NETs) and chronic inflammatory airwaydiseases.
DATA SOURCES: Articles published up to January 1, 2017, were selected from the PubMed, Ovid Medline, Embase databases, with the keywords of "asthma" or"pulmonary disease, chronic obstructive", "neutrophils" and "extracellulartraps."
STUDY SELECTION: Articles were obtained and reviewed to analyze the role of NETsin asthma and COPD.
RESULTS: NETs are composed of extracellular DNA, histones, and granular proteins,which are released from activated neutrophils. Multiple studies have indicatedthat there are a large amount of NETs in the airways of asthmatics and COPDpatients. NETs can engulf and kill invading pathogens in the host. However,disordered regulation of NET formation has shown to be involved in thedevelopment of asthma and COPD. An overabundance of NETs in the airways or lungtissue could cause varying degrees of damage to lung tissues by inducing thedeath of human epithelial and endothelial cells, and thus resulting in impairing pulmonary function and accelerating the progress of the disease.
CONCLUSIONS: Excessive NETs accumulate in the airways of asthmatics and COPD patients. Although NETs play an essential role in the innate immune system against infection, excessive components of NETs can cause lung tissue damage and accelerate disease progression in asthmatics and COPD patients. These findings suggest that administration of NETs could be a novel approach to treat asthma and COPD. Mechanism studies, clinical practice, and strategies to regulate neutrophil activation or directly interrupt NET function in asthmatics and COPD patients are desperately needed.
 
Chin Med J (Engl). 2017 Mar 20;130(6):730-736. doi: 10.4103/0366-6999.201608.





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