Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands.
Respir Res. 2010 Jul 22;11(1):99. doi: 10.1186/1465-9921-11-99.
Tobacco 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.
The 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.
The 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-1 alpha and TNF-alpha) 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.
The 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.
吸烟会刺激和损伤呼吸道，增加患肺气肿的风险。目前，戒烟是减缓肺气肿进展的唯一有效治疗方法，但是对于戒烟对气道细胞因子和趋化因子水平的影响知之甚少。据我们所知，这是第一项关于在停止吸烟后评估气道细胞因子谱的体内研究。
通过分析肺泡扩大、心脏肥大、支气管肺泡灌洗液（BALF）和肺组织中的炎性细胞以及通过确定暴露于香烟烟雾的 A/J 小鼠的 BALF 中的细胞因子和趋化因子谱，研究气道重塑和炎症的严重程度。烟雾暴露 20 周并在停止吸烟 8 周后。
暴露于香烟烟雾的小鼠中的肺泡扩大和右心室心脏肥大在停止吸烟后保持不变。尽管在停止吸烟后，暴露于香烟烟雾的动物的 BALF 中性粒细胞炎症减少，但肺组织中仍存在持续的炎症。暴露于香烟烟雾的小鼠 BALF 中升高的细胞因子（IL-1 alpha 和 TNF-alpha）和趋化因子（CCL2 和 CCL3）水平在停止吸烟后恢复到基础水平，而升高的 IL-12 水平未恢复到基础水平。香烟烟雾增强的 VEGF 水平在停止吸烟后没有明显变化。此外，暴露于香烟烟雾的小鼠的 BALF 中 IL-10 水平降低，与对照动物相比，这些水平在停止吸烟后仍明显降低。
暴露于香烟烟雾引起的气道炎症变化仅部分在停止吸烟后得到逆转。尽管戒烟应该是减缓肺气肿进展的第一步，但可以提供额外的药物来解决持续的气道炎症。
Zotero 插件
