Several epidemiological studies have identified the cigarette smoke as a risk factor for the infection and development of tuberculosis. Nicotine is considered the main immunomodulatory molecule of the cigarette. In the present study, we evaluated the effect of nicotine in the growth of M. tuberculosis. Lung epithelial cells and macrophages were infected with M. tuberculosis and/or treated with nicotine. The results show that nicotine increased the growth of M. tuberculosis mainly in type II pneumocytes (T2P) but not in airway basal epithelial cells nor macrophages. Further, it was observed that nicotine decreased the production of β-defensin-2, β-defensin-3, and the cathelicidin LL-37 in all the evaluated cells at 24 and 72 h post-infection. The modulation of the expression of antimicrobial peptides appears to be partially mediated by the nicotinic acetylcholine receptor α7 since the blockade of this receptor partially reverted the production of antimicrobial peptides. In summary, it was found that nicotine decreases the production of HBD-2, HBD-3, and LL-37 in T2P during the infection with M. tuberculosis promoting its intracellular growth.

中文翻译：

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尼古丁促进结核分枝杆菌在上皮细胞内生长

几项流行病学研究已将香烟烟雾确定为结核病感染和发展的危险因素。尼古丁被认为是香烟的主要免疫调节分子。在本研究中，我们评估了尼古丁对结核分枝杆菌生长的影响。肺上皮细胞和巨噬细胞被结核分枝杆菌感染和/或用尼古丁处理。结果表明，尼古丁主要促进了结核分枝杆菌在 II 型肺细胞 (T2P) 中的生长，但不增加气道基底上皮细胞和巨噬细胞的生长。此外，据观察，在感染后 24 小时和 72 小时，尼古丁降低了所有评估细胞中 β-防御素-2、β-防御素-3 和导管素 LL-37 的产生。抗菌肽表达的调节似乎部分由烟碱乙酰胆碱受体 α7 介导，因为该受体的阻断部分恢复了抗菌肽的产生。总之，发现尼古丁在感染结核分枝杆菌期间减少 T2P 中 HBD-2、HBD-3 和 LL-37 的产生，促进其细胞内生长。