Cigarette smoke facilitates allergen penetration across respiratory epithelium
Article first published online: 17 DEC 2008
DOI: 10.1111/j.1398-9995.2008.01861.x
© 2008 The Authors. Journal compilation © 2008 Blackwell Munksgaard
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How to Cite
Gangl, K., Reininger, R., Bernhard, D., Campana, R., Pree, I., Reisinger, J., Kneidinger, M., Kundi, M., Dolznig, H., Thurnher, D., Valent, P., Chen, K.-W., Vrtala, S., Spitzauer, S., Valenta, R. and Niederberger, V. (2009), Cigarette smoke facilitates allergen penetration across respiratory epithelium. Allergy, 64: 398–405. doi: 10.1111/j.1398-9995.2008.01861.x
Publication History
- Issue published online: 23 FEB 2009
- Article first published online: 17 DEC 2008
- Accepted for publication 7 July 2008
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Keywords:
- allergen penetration;
- cigarette smoke;
- permeability;
- recombinant allergens;
- respiratory epithelium
Background: The association between cigarette smoke exposure and allergic airway disease is a matter for debate. We sought to investigate in an in vitro system whether active smoking reduces the integrity and barrier function of the respiratory epithelium and thus facilitates allergen penetration.
Methods: We cultured the human bronchial epithelial cell line 16HBE14o− in a transwell culture system as a surrogate for the intact respiratory epithelium. The cell monolayer was exposed to standardized cigarette smoke extract (CSE). The extent and effects of trans-epithelial allergen penetration were measured using 125I-labelled purified major respiratory allergens (rBet v 1, rPhl p 5 and rDer p 2) and histamine release experiments.
Results: Exposure of cells to concentrations of CSE similar to those found in smokers induced the development of para-cellular gaps and a decrease in trans-epithelial resistance. CSE exposure induced a more than threefold increase in allergen penetration. Increased subepithelial allergen concentrations provoked a substantial augmentation of histamine release from sensitized basophils.
Conclusions: Our results indicate that cigarette smoke is a potent factor capable of reducing the barrier function of the respiratory epithelium for allergens and may contribute to increased allergic inflammation, exacerbation of allergic disease and boosting of IgE memory.

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