Abstract
Introduction: We have aimed to develop a mouse model of cigarette smoke (CS)-induced small airway disease and emphysema. This model will be used for studies of pathogenic responses in the development of emphysema and for preclinical evaluation of new drug candidates.
Methods: BALB/c mice were exposed to CS (nose-only), 5 days a week during 10 weeks (Gr.1: 6 cigarettes during 10 min, twice a day; Gr. 2: 12 cigarettes once a day during 20 min; Gr 3: 12 cigarettes during 20 min, twice a day; Gr 4: control, room air). The experiment ended on day 71-73 and day 85-87 (two additional recovery weeks without CS smoke) with thoroughly investigated lung mechanics (FlexiVent), inflammatory cell counts in bronchoalveolar lavage (BAL) and lung histology.
Results: CS induced an increased respiratory resistance (p<0.05), tissue resistance (p<0.05), tissue elastance (p<0.05), and decreased respiratory compliance (p<0.05), in all CS groups compared to control groups. However, there were no differences in lung mechanics and total cell counts in BAL within the CS-groups. After the recovery weeks, the CS-induced effects in the lung were sustained in all groups except for Gr 2. Lung histology showed no obvious alveolar damage in peripheral airways.
Conclusion: In our mouse model there is a marked effect on lung mechanics, suggesting that CS induce small airway inflammation which is not dose dependent. Our result indicates that it is the exposure time, rather than the number of cigarettes, that determines the detrimental effects in the mouse lung. Additionally, this model can be used for combined exposure of allergens and air-borne particulate pollution in order to investigate aggravating effects of inhaled particles on emphysema and COPD.
- © 2011 ERS
