Cigarette Smoke Condensate Inhibits Transepithelial Chloride Transport and Ciliary Beat Frequency
Cigarette Smoke Condensate Inhibits Transepithelial Chloride Transport and Ciliary Beat Frequency
复制标题
DOI：
10.1002/lary.20223
复制
发表时间：
2009-11-01
期刊：
影响因子：
2.6
通讯作者：
Woodworth, Bradford A.
中科院分区：
文献类型：
--
作者：
Cohen, Noam A.;Zhang, Shaoyan;Woodworth, Bradford A.
目的/假设：虽然导致鼻窦炎的病理生理学是复杂的，但证据表明粘膜纤毛清除率（MCC）降低是一个主要的贡献特征。正常呼吸道上皮MCC是一种重要的宿主防御机制，其依赖于适当的纤毛搏动和气道表面液体（ASL）的生物学特性。烟草烟雾暴露作为MCC抑制剂的作用尚未阐明。本研究调查香烟烟雾暴露对纤毛功能和transepithelial氯（Cl-）分泌的后果，ASL.Study设计的一个主要决定因素：在体外investigation.Methods：良好的特点主要小鼠鼻中隔上皮（MSE）和人鼻窦上皮（HSNE）文化暴露于香烟烟雾冷凝物（CSC），并与对照文化。采用药理学方法研究对纤毛搏动频率（CBF）和Cl-分泌的影响。毛喉素刺激电流（AISC）的变化，代表跨上皮Cl-分泌，在CSC暴露的MNSE中显著降低（14.97 +/- 1.2 μ A/cm（2）vs.对照，19.1 +/- 1.56 μ A/cm（2）[P = .04]）和HSNE（2.68 ± 0.79 μ A/cm（2）VS.对照，10.8 +/- 1.73 μ A/cm（2））培养物（P = .001）。毛喉素刺激的CBF也显着减少急性暴露于CSC（5.64 +/- 0.06 Hz与对照7.15 +/- 0.18 Hz）。结论：本研究提供了直接的证据表明，烟草烟雾减少MCC的两个主要组成部分。这将烟草烟雾作为慢性鼻窦炎暴露个体的潜在促成和/或加重因素联系起来。
Objectives/Hypothesis: Although the pathophysiology leading to rhinosinusitis is complex, evidence indicates that decreased mucociliary clearance (MCC) is a major contributing feature. Normal respiratory epithelial MCC is an important host defense mechanism that is dependent on proper ciliary beating and the biological properties of the airway surface liquid (ASL). The role that tobacco smoke exposure plays as an inhibitor of MCC has yet to be elucidated. The present study investigates the consequences of cigarette smoke exposure on ciliary function and transepithelial chloride (Cl-) secretion, a major determinant of ASL.Study Design: In vitro investigation.Methods: Well-characterized primary murine nasal septal epithehal (MNSE) and human sinonasal epithelial (HSNE) cultures were exposed to cigarette smoke condensate (CSC) and compared to control cultures. Effects on ciliary beat frequency (CBF) and Cl- secretion were investigated using pharmacologic manipulation.Results: Change in forskolin-stimulated current (AISC), representing transepithelial Cl- secretion, was significantly decreased in CSC exposed MNSE (14.97 +/- 1.2 mu A/cm(2) vs. control, 19.1 +/- 1.56 mu A/cm(2) [P = .04]) and HSNE (2.68 0.79 mu A/cm(2) VS. control, 10.8 +/- 1.73 mu A/cm(2)) cultures (P = .001). Forskolin-stimulated CBF was also significantly reduced when acutely exposed to CSC (5.64 +/- 0.06 Hz vs. control 7.15 +/- 0.18 Hz).Conclusions: The present study provides direct evidence that tobacco smoke diminishes two major components of MCC. This links tobacco smoke as a potential contributing and/or exacerbating factor in exposed individuals with chronic rhinosinusitis.