Inflammatory changes in the airways of mice caused by cigarette smoke exposure are only partially reversed after smoking cessation.
Inflammatory changes in the airways of mice caused by cigarette smoke exposure are only partially reversed after smoking cessation.
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DOI：
10.1186/1465-9921-11-99
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发表时间：
2010-07-22
影响因子：
5.8
通讯作者：
Folkerts G
中科院分区：
文献类型：
--
作者：
Braber S;Henricks PA;Nijkamp FP;Kraneveld AD;Folkerts G
吸烟会刺激和损害呼吸道，增加患肺气肿的风险。目前，戒烟是减少肺气肿进展的唯一有效治疗方法，然而，关于戒烟对气道中细胞因子和趋化因子水平的影响几乎一无所知。据我们所知，这是第一次报告的体内研究，其中细胞因子的档案，确定后停止吸烟暴露。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测定暴露于香烟烟雾20周和戒烟后8周的A/J小鼠的BALF中的细胞因子和趋化因子谱来研究气道重塑和炎症的严重程度。吸烟小鼠的肺泡增大和右心室肥大在戒烟后保持不变。虽然香烟烟雾暴露的动物的BALF中的嗜酸性炎症在戒烟后减少，但观察到肺组织中的持续炎症。吸烟小鼠BALF中升高的细胞因子（IL-1α和TNF-α）和趋化因子（CCL 2和CCL 3）水平在戒烟后恢复至基础水平，而升高的IL-12水平未恢复至基础水平。戒烟后香烟烟雾增强的VEGF水平没有显着变化。此外，IL-10水平降低，在BALF中的烟雾暴露的小鼠和这些水平仍然显着降低后，戒烟相比，对照组动物。吸烟引起的气道炎症变化在戒烟后仅部分逆转。虽然戒烟应该是减少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。
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-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. 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.
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影响因子：
3.3
作者：
Bisset, LR;Schmid-Grendelmeier, P
通讯作者：
Schmid-Grendelmeier, P
影响因子：
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BRUNNEMANN, KD;HOFFMANN, D
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HOFFMANN, D
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作者：
D'hulst, AI;Vermaelen, KY;Pauwels, RA
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