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Cigarette smoke condensate inhibits transepithelial chloride transport and ciliary beat frequency

✍ Scribed by Noam A. Cohen; Shaoyan Zhang; Dawn B. Sharp; Edwin Tamashiro; Bei Chen; Eric J. Sorscher; Bradford A. Woodworth


Book ID
102447038
Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
326 KB
Volume
119
Category
Article
ISSN
0023-852X

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✦ Synopsis


Abstract

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 epithelial (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 (ΔI~SC~), representing transepithelial Cl^−^ secretion, was significantly decreased in CSC exposed MNSE (14.97 ± 1.2 μA/cm^2^ vs. control, 19.1 ± 1.56 μA/cm^2^ [P = .04]) and HSNE (2.68 ± 0.79 μA/cm^2^ vs. control, 10.8 ± 1.73 μA/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. Laryngoscope, 2009


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## Abstract ## Objectives/Hypothesis: The cystic fibrosis transmembrane conductance regulator (CFTR) serves as a predominant Cl^−^ transport conduit in airway epithelium and is inhibited by cigarette smoke in vitro and in vivo. Activation of secondary Cl^−^ transport pathways through calcium‐activ