The Pulmonary Center, Boston University Medical Center, 72 East Concord Street R-304, Boston, MA 02118.
Proc Am Thorac Soc. 2009 Dec;6(8):697-700. doi: 10.1513/pats.200907-076DP.
Although cigarette smoking is the major cause of chronic obstructive pulmonary disease (COPD), only a subset of smokers develops this disease. There is significant clinical, radiographic, and pathologic heterogeneity within smokers who develop COPD that likely reflects multiple molecular mechanisms of disease. It is possible that variations in the individual response to cigarette smoking form the basis for the distinct clinical and molecular phenotypes and variable natural history associated with COPD. Using the biologic premise of a molecular field of airway injury created by cigarette smoking, this response to tobacco exposure can be measured by molecular profiling of the airway epithelium. Noninvasive study of this field effect by profiling 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.
虽然吸烟是慢性阻塞性肺疾病（COPD）的主要原因，但只有一部分吸烟者会患上这种疾病。在患有 COPD 的吸烟者中，存在显著的临床、影像学和病理学异质性，这可能反映了疾病的多种分子机制。吸烟引起的个体反应的差异可能是 COPD 相关的不同临床和分子表型以及不同自然史的基础。利用吸烟引起的气道损伤的分子场这一生物学前提，可以通过气道上皮的分子谱分析来测量对烟草暴露的这种反应。通过对 COPD 患者的气道基因表达进行分子谱分析来无创性地研究这种场效应，对我们理解疾病异质性、早期疾病检测和识别新的疾病修饰治疗具有重要意义。
