title: Effect of smoking cessation on airway inflammation of rats with chronic bronchitis.
abstract: BACKGROUND
  Smoking is the major cause of airway inflammation in chronic obstructive pulmonary disease (COPD), and smoking cessation is regarded as one of the important strategies for prevention and treatment of the inflammation. The inflammation of the chronic airway may be present and deteriorated even if the COPD patients stop smoking. Whether and how early smoking cessation affects the progress of inflammation is still obscure. This study was conducted to find the appropriate time for smoking cessation to terminate the airway inflammation in rats with smoke-induced chronic bronchitis.
  
  
  METHODS
  A rat model of COPD was established by passively inhaling smoke mixture. Fifty-four young male Sprague-Dawley rats were randomly divided into 9 groups with different periods of smoke exposure and different time points of cessation. The inflammation markers to be detected included inflammatory cells in the bronchoalveolar lavage fluid (BALF), the myeloperoxidose (MPO) activity, the morphologic changes and the expression of ICAM-1 on the airway epithelium.
  
  
  RESULTS
  When smoking was terminated at early stage, the inflammatory markers and related indexes were different from those of the typical chronic bronchitis group (group M7) (P < 0.01). The pathologic score of group SC7 (2 weeks of smoking cessation after occurrence of typical chronic bronchitis) was not different from that of group M7, and the level of ICAM-1 was still up-regulated (compared to group M7, P > 0.05). Meanwhile, most of inflammatory cells in BALF were neutrophils compared to other groups (P < 0.01). When smoking was terminated, the MPO activity was significantly lower than that of group M7 (P < 0.01).
  
  
  CONCLUSIONS
  Smoking cessation at early stage can effectively inhibit the inflammatory reaction of COPD. Once chronic bronchitis occurs, little could be improved by smoking cessation.
authors.affiliation: Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. liqingyun68@yahoo.com.cn
authors.forename: Qing-yun
authors.initials: QY
authors.lastname: Li
authors.forename: Shao-guang
authors.initials: SG
authors.lastname: Huang
authors.forename: Huan-ying
authors.initials: HY
authors.lastname: Wan
authors.forename: Hua-cheng
authors.initials: HC
authors.lastname: Wu
authors.forename: Tong
authors.initials: T
authors.lastname: Zhou
authors.forename: Min
authors.initials: M
authors.lastname: Li
authors.forename: Wei-wu
authors.initials: WW
authors.lastname: Deng
mesh_terms: D000818:Animals; D001991:Bronchitis / Q000473:pathology*; D002908:Chronic Disease; D007249:Inflammation / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008168:Lung / Q000473:pathology*; D008297:Male; D009504:Neutrophils / Q000502:physiology; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016540:Smoking Cessation
chemical_list: D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase