Toll样受体在慢性阻塞性肺疾病发病机制中的作用

Mechanisms of role of Toll-like receptors in the pathogenesis of chronic obstructive pulmonary disease

慢性阻塞性肺疾病(COPD)是一种以气道炎症为主要标志的慢性呼吸系统疾病。而COPD气道炎症的启动、激发和炎性信号级联放大机制尚不甚明了。近年来研究表明模式识别受体(PRRs)在COPD慢性炎症的启动和维持过程中扮演着重要角色。其中,尤以Toll样受体(TLRs)与COPD发病关系最为密切。吸烟、有害气体、微生物及损伤相关分子模式(DAMPs)与TLRs相互作用,通过NF-κB信号转导通路完成跨膜信号转导,最终调节炎症基因的转录和翻译,产生大量炎症介质并趋化大量炎症细胞参与气道炎症反应的启动及维持。本文结合近年来国内外的最新相关研究成果,对TLRs及下游信号转导通路在COPD发病机制中的重要作用综述如下。

Chronic obstructive pulmonary disease（COPD） is one of chronic respiratory disease characterized by airway inflammation. However, the mechanism of the initiation and trigger and cascade of inflammation responses is still not clear. In recent years, pattern recognition receptors（PRRs）, especially Toll-like receptors（TLRs） are thought as key players in the initiation and sustaining of inflammatory responses in patients with COPD. TLRs interact with cigarette smoke（CS）, noxious gases, pathogen- associated molecular patterns（PAMPs） and damage associate molecular patterns（DAMPs） that are released in response to cell injury. Transmembrane signal transduction through NF-κB pathway leads to persistent airway inflammation via transcription and translation of inflammatory genes, formation and release of pro-inflammatory cytokines and chemokines as well as neutrophils with other inflammatory active cells recruited. Combining the domestic and foreign research results, this review will explore TLR and molecular signaling pathway and their potential roles in COPD.