Division of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA 92697, USA.
Mediators Inflamm. 2020 Feb 29;2020:6705428. doi: 10.1155/2020/6705428. eCollection 2020.
Smoking is a major risk factor for pulmonary diseases that include chronic obstructive pulmonary diseases (COPD) and cancer. Nicotine is the toxic and addictive component of tobacco products, like cigarettes, that negatively affects the immune system. Here, we examined the effect of nicotine on the IL-22 pathway that protects lung function by increasing transepithelial resistance and epithelial cell regeneration and repair. Our results indicate that exposure to nicotine impairs the regenerative capacity of primary bronchial epithelial cells in scratch assays. IL-22 at 100 ng/ml significantly improved wound healing in epithelial cells; however, the exposure to nicotine hampered the IL-22-mediated effect of wound healing. Investigation into the mechanisms showed that IL-22 receptor, IL-22R1, was downregulated in the presence of nicotine as determined by q-PCR and flow cytometry. We also investigated the effect of nicotine on IL-22 production by T cells. Results indicate that nicotine inhibited the secretion of IL-22 from T cells in response to aryl hydrocarbon receptor (AHR) ligand, FICZ. Altogether, the data suggests that nicotine negatively influences the IL-22-IL-22R axis. This impairment may contribute to the nicotine-mediated detrimental effects on lung function.
吸烟是肺部疾病的主要风险因素，包括慢性阻塞性肺疾病（COPD）和癌症。尼古丁是香烟等烟草制品中的有毒和成瘾成分，会对免疫系统产生负面影响。在这里，我们研究了尼古丁对 IL-22 途径的影响，该途径通过增加上皮细胞的跨上皮阻力和再生和修复来保护肺功能。我们的结果表明，暴露于尼古丁会损害划痕实验中原发性支气管上皮细胞的再生能力。100ng/ml 的 IL-22 显著改善了上皮细胞的伤口愈合；然而，尼古丁暴露阻碍了 IL-22 介导的伤口愈合作用。对机制的研究表明，q-PCR 和流式细胞术检测到尼古丁存在时，IL-22 受体 IL-22R1 下调。我们还研究了尼古丁对 T 细胞产生 IL-22 的影响。结果表明，尼古丁抑制了 T 细胞对芳基烃受体（AHR）配体 FICZ 反应时 IL-22 的分泌。总之，数据表明尼古丁会对 IL-22-IL-22R 轴产生负面影响。这种损伤可能导致尼古丁对肺功能的有害影响。
