中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
4期
726-728
,共3页
肺疾病,慢性阻塞性%Toll样受体%信号传导%气道炎症
肺疾病,慢性阻塞性%Toll樣受體%信號傳導%氣道炎癥
폐질병,만성조새성%Toll양수체%신호전도%기도염증
Pulmonary disease,chronic obstructive%Toll-like receptors%Signal transduction%Airway inflammation
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。
慢性阻塞性肺疾病（COPD）是一種以氣道炎癥為主要標誌的慢性呼吸繫統疾病。而COPD 氣道炎癥的啟動、激髮和炎性信號級聯放大機製尚不甚明瞭。近年來研究錶明模式識彆受體（PRRs）在COPD慢性炎癥的啟動和維持過程中扮縯著重要角色。其中，尤以Toll樣受體（TLRs）與COPD髮病關繫最為密切。吸煙、有害氣體、微生物及損傷相關分子模式（DAMPs）與TLRs相互作用，通過NF-κB信號轉導通路完成跨膜信號轉導，最終調節炎癥基因的轉錄和翻譯，產生大量炎癥介質併趨化大量炎癥細胞參與氣道炎癥反應的啟動及維持。本文結閤近年來國內外的最新相關研究成果，對TLRs及下遊信號轉導通路在COPD髮病機製中的重要作用綜述如下。
만성조새성폐질병（COPD）시일충이기도염증위주요표지적만성호흡계통질병。이COPD 기도염증적계동、격발화염성신호급련방대궤제상불심명료。근년래연구표명모식식별수체（PRRs）재COPD만성염증적계동화유지과정중분연착중요각색。기중，우이Toll양수체（TLRs）여COPD발병관계최위밀절。흡연、유해기체、미생물급손상상관분자모식（DAMPs）여TLRs상호작용，통과NF-κB신호전도통로완성과막신호전도，최종조절염증기인적전록화번역，산생대량염증개질병추화대량염증세포삼여기도염증반응적계동급유지。본문결합근년래국내외적최신상관연구성과，대TLRs급하유신호전도통로재COPD발병궤제중적중요작용종술여하。
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.
