Bronchial epithelial cells: The key effector cells in the pathogenesis of chronic obstructive pulmonary disease?
Bronchial epithelial cells: The key effector cells in the pathogenesis of chronic obstructive pulmonary disease?
复制标题
支气管上皮细胞：慢性阻塞性肺疾病发病机制中的关键效应细胞？
DOI：
10.1111/resp.12542
复制
发表时间：
2015-07-01
期刊：
影响因子：
--
通讯作者：
Yao, Xin
中科院分区：
文献类型：
--
作者：
Gao, Wei;Li, Lingling;Yao, Xin
The primary function of the bronchial epithelium is to act as a defensive barrier aiding the maintenance of normal airway function. Bronchial epithelial cells (BEC) form the interface between the external environment and the internal milieu, making it a major target of inhaled insults. However, BEC can also serve as effectors to initiate and orchestrate immune and inflammatory responses by releasing chemokines and cytokines, which recruit and activate inflammatory cells. They also produce excess reactive oxygen species as a result of an oxidant/antioxidant imbalance that contributes to chronic pulmonary inflammation and lung tissue damage. Accumulated mucus from hyperplastic BEC obstructs the lumen of small airways, whereas impaired cell repair, squamous metaplasia and increased extracellular matrix deposition underlying the epithelium is associated with airway remodelling particularly fibrosis and thickening of the airway wall. These alterations in small airway structure lead to airflow limitation, which is critical in the clinical diagnosis of chronic obstructive pulmonary disease (COPD). In this review, we discuss the abnormal function of BEC within a disturbed immune homeostatic environment consisting of ongoing inflammation, oxidative stress and small airway obstruction. We provide an overview of recent insights into the function of the bronchial epithelium in the pathogenesis of COPD and how this may provide novel therapeutic approaches for a number of chronic lung diseases.
