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2609679 
Journal Article 
Abstract 
Cigarette smoke attenuates house dust mite induced allergic airway inflammation in mice 
Staempfli, MR; Llop-Guevara, A; Trimble, NJ; Nikota, JK; Bauer, CM; Kianpour, S; Botelho, FM 
2010 
Yes 
American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970 
181 
A2819 
English 
WOS:000208771001731 
is part of a larger document 3452678 Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Rationale: In most developed countries, approximately 25% of asthmatic individuals are current smokers. Despite this, the impact of active smoking on immune inflammatory processes and tissue remodeling associated with allergic airway inflammation remains poorly understood. Also, most animal studies that have studied the impact of cigarette smoke on allergic airway inflammation utilized ovalbumin, an innocuous egg antigen that unlike complex allergen extracts does not elicit an allergic inflammatory response on its own.

Aims: The objective of this study was to investigate the impact of cigarette smoke on airway inflammation and tissue remodeling using a model of house dust mite (HDM)-induced allergic airway inflammation.

Methods: BALB/c mice were inoculated intranasally with HDM daily, five days per week, for 3 weeks to establish chronic airway inflammation. Subsequently mice were concurrently exposed to HDM plus cigarette smoke for 2 weeks using a whole body cigarette smoke exposure system. As controls we included room air (sham) and smoke only exposed animals, and sham exposed animals that were inoculated with HDM.

Results: We observed significantly attenuated airway eosinophilia in mice exposed to HDM plus cigarette smoke compared to HDM only exposed animals. Cigarette smoke exposure also attenuated HDM-induced increases in the percentage of activated (CD69+) B cells and serum HDM-specific IgE levels, while having no effect on CD69+ or IL-5+ CD4 T cells. We further observed decreased mucus staining (PAS plus Alcian blue (pH 2.5)) in tissue section from HDM plus cigarette smoke compared to HDM only exposed animals. While collagen deposition increased, smooth muscle actin staining remained unchanged between HDM plus smoke and HDM only exposed animals. Analysis of lung physiology revealed a similar increase in airway resistance in HDM exposed animals and mice that were concurrently exposed to HDM plus cigarette smoke. Of note, tissue resistance and elasticity was markedly decreased in mice concurrently exposed to HDM plus cigarette smoke.

Conclusions: Our findings clearly show that cigarette smoke attenuates inflammatory processes associated with allergic airway inflammation. Interestingly, attenuated inflammation is associated with increased collagen deposition. Studies are ongoing investigating the underlying mechanisms. 
American Thoracic Society 2010 International Conference 
New Orleans, LA 
May 14-19, 2010