Smoking-induced gene expression changes in the bronchial airway are reflected in nasal and buccal epithelium.
Smoking-induced gene expression changes in the bronchial airway are reflected in nasal and buccal epithelium.
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吸烟引起的基因表达在支气管气道中的变化反映在鼻和颊上皮中。
DOI：
10.1186/1471-2164-9-259
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发表时间：
2008-05-30
期刊：
影响因子：
4.4
通讯作者：
Spira, Avrum
中科院分区：
文献类型：
--
作者：
Sridhar, Sriram;Schembri, Frank;Zeskind, Julie;Shah, Vishal;Gustafson, Adam M.;Steiling, Katrina;Liu, Gang;Dumas, Yves-Martine;Zhang, Xiaohui;Brody, Jerome S.;Lenburg, Marc E.;Spira, Avrum
吸烟是可预防死亡的主要原因，也是肺癌和慢性阻塞性肺病的重要原因。先前的研究已经证明，吸烟在暴露于香烟烟雾的整个气道上皮中产生分子损伤场。我们以前的特点是基因表达在支气管上皮从不吸烟者，并确定了基因表达的变化，发生在主支气管吸烟。在这项研究中，我们探讨了健康的当前和从不吸烟者的胸外（颊和鼻）和胸内（支气管）上皮细胞之间全基因组基因表达的关系。使用先前定义为在从不吸烟者的支气管气道中表达的基因（“正常气道转录组”），我们发现，与其他上皮和非上皮组织相比，非吸烟者的支气管和鼻上皮在基因表达方面最相似，其中几种抗氧化剂，解毒和结构基因在支气管和鼻子中都高度表达。主成分分析先前定义的吸烟诱导的基因从支气管表明，吸烟对鼻上皮细胞的基因表达有类似的影响。基因集富集分析表明，这组基因也高度富集在鼻和颊上皮样本中吸烟改变最多的基因中。在所有三种呼吸道上皮组织中，吸烟通常会改变几种解毒基因的表达，这表明对烟草暴露的共同气道反应。我们的研究结果支持胸外和胸内气道上皮细胞的基因表达之间的关系，并扩展了吸烟诱导的口腔和鼻腔上皮细胞损伤领域的概念。这种关系可能被用来开发一种非侵入性的生物标志物，烟草暴露以及非侵入性的筛选或诊断工具，提供有关个人吸烟引起的肺部疾病的易感性的信息。
Cigarette smoking is a leading cause of preventable death and a significant cause of lung cancer and chronic obstructive pulmonary disease. Prior studies have demonstrated that smoking creates a field of molecular injury throughout the airway epithelium exposed to cigarette smoke. We have previously characterized gene expression in the bronchial epithelium of never smokers and identified the gene expression changes that occur in the mainstem bronchus in response to smoking. In this study, we explored relationships in whole-genome gene expression between extrathorcic (buccal and nasal) and intrathoracic (bronchial) epithelium in healthy current and never smokers. Using genes that have been previously defined as being expressed in the bronchial airway of never smokers (the "normal airway transcriptome"), we found that bronchial and nasal epithelium from non-smokers were most similar in gene expression when compared to other epithelial and nonepithelial tissues, with several antioxidant, detoxification, and structural genes being highly expressed in both the bronchus and nose. Principle component analysis of previously defined smoking-induced genes from the bronchus suggested that smoking had a similar effect on gene expression in nasal epithelium. Gene set enrichment analysis demonstrated that this set of genes was also highly enriched among the genes most altered by smoking in both nasal and buccal epithelial samples. The expression of several detoxification genes was commonly altered by smoking in all three respiratory epithelial tissues, suggesting a common airway-wide response to tobacco exposure. Our findings support a relationship between gene expression in extra- and intrathoracic airway epithelial cells and extend the concept of a smoking-induced field of injury to epithelial cells that line the mouth and nose. This relationship could potentially be utilized to develop a non-invasive biomarker for tobacco exposure as well as a non-invasive screening or diagnostic tool providing information about individual susceptibility to smoking-induced lung diseases.
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