摘要
肺泡上皮细胞和巨噬细胞的相互作用受到了肺组织的严格调控,而细胞间通信(cellular crosstalk)的失衡往往导致多种肺部疾病的发生。特发性肺纤维化(idiopathic pulmonary fibrosis,IPF)是一种慢性呼吸系统疾病,其特征为肺部胶原过度沉积。肺泡上皮细胞与巨噬细胞在肺纤维化的局部炎症反应中扮演着重要的角色。损伤后的肺泡上皮细胞会启动一系列免疫应答,以此修复肺组织结构,然而,在IPF中免疫环境的紊乱往往导致修复方向的转变。这种紊乱可能导致炎症反应的持续存在,进而促进纤维化过程的进行,最终导致肺组织的瘢痕化和功能受损。目前尚不清楚IPF中异常的细胞交互如何导致病理性修复,因此,探究肺泡上皮细胞与巨噬细胞的相互作用可能为IPF的治疗提供新的思路。现就肺泡上皮细胞屏障的损伤与巨噬细胞过度激活的机制及二者间信号的传递如何影响肺部促纤维化环境作一概述。
The precise communication between alveolar epithelial cells and macrophages is critical in maintaining pulmonary homeostasis,and any disturbance in this intricate interplay has been closely linked to various pulmonary diseases.Among these diseases,idiopathic pulmonary fibrosis(IPF) is a chronic respiratory disorder characterized by excessive collagen deposition,which involves complex interactions between alveolar epithelial cells and macrophages.Following injury,alveolar epithelial cells initiate a series of immune responses to repair lung tissue architecture.However,in IPF,dysregulation of the immune environment often leads to aberrant repair.Such disturbance may cause persistence of inflammatory reactions,which promotes fibrogenesis,ultimately resulting in lung scarring and impaired function.Despite extensive research,the exact roles of disrupted communication between these cells in pathological wound healing remain poorly understood.Hence,a comprehensive understanding of the interplays between these cells could potentially lead to the development of novel therapeutic strategies.This review examines the mechanisms of damaged alveolar epithelium and the activation of pro-fibrotic macrophages.We also aim to explore the communication between epithelial cells and macrophages that underlies the formation of a pro-fibrotic milieu.
作者
杜欣倩(综述)
崔烨(审校)
DU Xinqian;CUI Ye(Department of Immunology,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China)
出处
《微生物学免疫学进展》
CAS
2023年第5期61-67,共7页
Progress In Microbiology and Immunology
基金
国家自然科学基金(81974050)
北京市教育委员会科技计划一般项目(KM202010025003)。
关键词
肺纤维化
肺泡上皮细胞
上皮间充质转化
巨噬细胞
极化
细胞互作
肺损伤修复
2型免疫
Pulmonary fibrosis
Alveolar epithelial cell
Epithelial-mesenchymal transition
Macrophage
Polarization
Cellular crosstalk
Lung repair
Type 2 immunity