Abstract
BackgroundTobacco smoking irritates and damages the respiratory tract and contributes to a higher risk of developing lung emphysema. At present, smoking cessation is the only effective treatment for reducing the progression of lung emphysema, however, there is hardly anything known about the effects of smoking cessation on cytokine and chemokine levels in the airways. To the best of our knowledge, this is the first reported in vivo study in which cytokine profiles were determined after cessation of cigarette smoke exposure.MethodsThe severity of airway remodeling and inflammation was studied by analyzing alveolar enlargement, heart hypertrophy, inflammatory cells in the bronchoalveolar lavage fluid (BALF) and lung tissue and by determining the cytokine and chemokine profiles in the BALF of A/J mice exposed to cigarette smoke for 20 weeks and 8 weeks after smoking cessation.ResultsThe alveolar enlargement and right ventricle heart hypertrophy found in smoke-exposed mice remained unchanged after smoking cessation. Although the neutrophilic inflammation in the BALF of cigarette smoke-exposed animals was reduced after smoking cessation, a sustained inflammation in the lung tissue was observed. The elevated cytokine (IL-1α and TNF-α) and chemokine (CCL2 and CCL3) levels in the BALF of smoke-exposed mice returned to basal levels after smoking cessation, while the increased IL-12 levels did not return to its basal level. The cigarette smoke-enhanced VEGF levels did not significantly change after smoking cessation. Moreover, IL-10 levels were reduced in the BALF of smoke-exposed mice and these levels were still significantly decreased after smoking cessation compared to the control animals.ConclusionThe inflammatory changes in the airways caused by cigarette smoke exposure were only partially reversed after smoking cessation. Although smoking cessation should be the first step in reducing the progression of lung emphysema, additional medication could be provided to tackle the sustained airway inflammation.
Highlights
There are currently more than 1.3 billion tobacco smokers worldwide according to the World Health Organization (WHO) [1]
The severity of airway remodeling and inflammation was studied by determining alveolar enlargement, heart hypertrophy, inflammatory cells in the bronchoalveolar lavage fluid (BALF) and lung tissue and by analyzing the cytokine and chemokine profiles in the BALF of mice exposed to cigarette smoke for 20 weeks and 8 weeks after smoking cessation
Right ventricle heart hypertrophy was not reversible after a period of 8 weeks without cigarette smoke exposure, because the heart hypertrophy ratio (RV/LV +S) was not significantly decreased in the smoking cessation group compared to smoke-exposed group
Summary
There are currently more than 1.3 billion tobacco smokers worldwide according to the World Health Organization (WHO) [1]. Migration and activation of inflammatory cells to the lung is regulated by the release of different mediators, including proteases, cytokines and chemokines secreted by a variety of inflammatory and resident cells These mediators contribute to the chronic inflammatory process with tissue damage and repair processes seen in emphysema [15,16]. There is insufficient evidence regarding the effects of smoking cessation on cytokine and chemokine levels, which do play an important role in airway inflammation and tissue remodeling seen in COPD. The severity of airway remodeling and inflammation was studied by determining alveolar enlargement, heart hypertrophy, inflammatory cells in the bronchoalveolar lavage fluid (BALF) and lung tissue and by analyzing the cytokine and chemokine profiles in the BALF of mice exposed to cigarette smoke for 20 weeks and 8 weeks after smoking cessation. To the best of our knowledge, this is the first reported in vivo study in which cytokine profiles were determined after cessation of cigarette smoke exposure
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