国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2011年
17期
1323-1327
,共5页
李丹%徐治波%王鸿程%雷建波
李丹%徐治波%王鴻程%雷建波
리단%서치파%왕홍정%뢰건파
气道基因表达%慢性阻塞性肺疾病%生物信息学
氣道基因錶達%慢性阻塞性肺疾病%生物信息學
기도기인표체%만성조새성폐질병%생물신식학
Airway gene expression%Chronic obstructive pulmonary disease%Bioinformatics
慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种具有气流受限特征的可以预防和治疗的疾病,气流受限不完全可逆、呈进行性发展,与肺部对香烟烟雾等有害气体或有害颗粒的异常炎症反应有关。COPD患病率及致残率高,吸烟为目前公认的危险因素,然而仅一部分吸烟者才发展成为本病,说明遗传因素在COPD的发病中起着重要作用。吸烟可诱导气道基因表达水平的改变,导致其编码蛋白组成的代谢及其调节系统功能异常,并最终可引起COPD的发生。多种研究方法为基因芯片技术分析吸烟诱导的气道上皮细胞的基因表达的改变,从而测量气道对烟草暴露的反应。在了解COPD的疾病异质性、早期发现疾病以及对新型改善COPD病情的治疗方法的认可方面,分析COPD患者的气道基因表达有着重要的意义。
慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一種具有氣流受限特徵的可以預防和治療的疾病,氣流受限不完全可逆、呈進行性髮展,與肺部對香煙煙霧等有害氣體或有害顆粒的異常炎癥反應有關。COPD患病率及緻殘率高,吸煙為目前公認的危險因素,然而僅一部分吸煙者纔髮展成為本病,說明遺傳因素在COPD的髮病中起著重要作用。吸煙可誘導氣道基因錶達水平的改變,導緻其編碼蛋白組成的代謝及其調節繫統功能異常,併最終可引起COPD的髮生。多種研究方法為基因芯片技術分析吸煙誘導的氣道上皮細胞的基因錶達的改變,從而測量氣道對煙草暴露的反應。在瞭解COPD的疾病異質性、早期髮現疾病以及對新型改善COPD病情的治療方法的認可方麵,分析COPD患者的氣道基因錶達有著重要的意義。
만성조새성폐질병(chronic obstructive pulmonary disease,COPD)시일충구유기류수한특정적가이예방화치료적질병,기류수한불완전가역、정진행성발전,여폐부대향연연무등유해기체혹유해과립적이상염증반응유관。COPD환병솔급치잔솔고,흡연위목전공인적위험인소,연이부일부분흡연자재발전성위본병,설명유전인소재COPD적발병중기착중요작용。흡연가유도기도기인표체수평적개변,도치기편마단백조성적대사급기조절계통공능이상,병최종가인기COPD적발생。다충연구방법위기인심편기술분석흡연유도적기도상피세포적기인표체적개변,종이측량기도대연초폭로적반응。재료해COPD적질병이질성、조기발현질병이급대신형개선COPD병정적치료방법적인가방면,분석COPD환자적기도기인표체유착중요적의의。
Chronic obstructive pulmonary disease (COPD)is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. Prevalence and disability of COPD is high. We have known that although cigarette smoking is risk factor for COPD, only some cigarette smokers go on to get COPD, suggesting that hereditary factor plays an important role in the pathogenesis of COPD. Smoking can be induced the gene expression level of changes in the airway, which cause the composed of the coding protein metabolism and its control system of abnormal function and finally can cause COPD happening. A variety of research methods are gene chip technology that analyse gene expression change in smoking-induced airway epithelial cell, to measure airway response to tobacco exposure. The analysis of airway gene expression in patients with COPD holds important implications for our understanding of disease heterogeneity, early disease detection, and identification of novel disease-modifying therapies.