吸烟对正常大鼠和卵清蛋白致敏大鼠支气管上皮细胞的改变存在差异
2009/10/15
背景：吸烟人类普遍的习惯，即使是哮喘患者也一样。支气管上皮细胞是暴露与刺激环境，如吸烟的第一道细胞屏障。这些细胞能产生诸多介质参与炎症和气道重构。然而，慢性烟雾暴露对这些介质的产生和释放的作用尚不清楚。
目的：通过研究对照和哮喘大鼠研究反复烟雾暴露对支气管上皮细胞介质分泌的影响。
方法：从正常大鼠（NRBE）和哮喘大鼠（卵清蛋白致敏，ARBE）中分离支气管上皮细胞。将细胞暴露于经AGI-30处理获得的香烟烟雾提取物（CSE）中。每天向培养基中加入3％CSE，连续5天。取基线及5天处理后的上清液。采用酶联免疫分析（ELISA）检测巨噬细胞趋化蛋白（MCP）-1、白介素（IL）-10、血管内皮生长因子（VEGF）、肿瘤坏死因子（TNF）、IL-1α及干扰素（IFN）-γ水平。
结果：TNF、IL-1α、IFN-γ低于检测下限。与ARBE 相比，基线时NRBE产生的MCP-1较少，但IL-10和VEGF较多。CSE暴露能降低NRBE IL-10的产生，但不能显著改变MCP-1和VEGF的产生。有趣的是，哮喘大鼠支气管上皮细胞对CSE的反应并不一致。在ARBE，CSE暴露后MCP-1水平下降 而VEGF水平上升，IL-10水平则无显著变化。
结论：与对照组相比，从哮喘大鼠分离的支气管上皮细胞能产生不同水平的介质，而且这些细胞对CSE暴露的反应也不相同。
（林江涛 审校）
St-Laurent J, et al. J Asthma. 2009 Aug;46(6):577-581.
Cigarette smoke differently alters normal and ovalbumin-sensitized bronchial epithelial cells from rat.
St-Laurent J, Boulet LP, Bissonnette E.
BACKGROUND: Smoking is a common habit in the general population, even in asthmatic patients. Bronchial epithelial cells are the first cellular elements exposed to environmental stimuli such as cigarette smoke. These cells produce a wide range of mediators involved in inflammation and remodeling processes. However, the effects of chronic smoke exposure on the release and production of these mediators remain unclear.
OBJECTIVES: To investigate the effects of repeated exposure to cigarette smoke extract on mediator released by bronchial epithelial cells isolated from control and asthmatic rats.
METHODS: Bronchial epithelial cells were isolated from normal (NRBE) and asthmatic rats (ARBE) (ovalbumin (OVA)-sensitized rat). Cells were exposed to cigarette smoke extract (CSE) obtained by impacting cigarette smoke with an AGI-30. A concentration of 3% CSE was added in the medium daily, for 5 consecutive days. Supernatant was recovered at baseline and after the 5 days. Levels of macrophage chemoattractant protein (MCP)-1, interleukin (IL)-10, vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF), IL-1alpha, and interferon (IFN)-gamma were measured using enzyme-linked immunosorbent assay (ELISA).
RESULTS: TNF, IL-1alpha, and IFN-gamma were lower than the detection limit of our methods. At the baseline, NRBE produced less MCP-1 but more IL-10 and VEGF when compared with ARBE. CSE exposure reduced NRBE IL-10 production but did not significantly alter MCP-1 and VEGF production. Interestingly, bronchial epithelial cells of asthmatic rats responded differently to CSE. MCP-1 level was decreased and VEGF increased after CSE exposure, whereas IL-10 level did not change in ARBE.
CONCLUSION: Cells isolated from asthmatic rats produced distinct levels of mediators compared with cells isolated from control rats. Furthermore, these cells react differently to CSE exposure.
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