目的探讨甲醛染毒对人支气管上皮细胞(16HBE细胞)炎性细胞因子表达的影响。方法以0、0.04、0.08、0.16、0.32、O.64mmol/L浓度的甲醛处理16HBE细胞,培养24h后四甲基偶氮唑盐微量酶反应比色法(MTT)法测定细胞的增殖活性并计算LD50;不同剂量甲醛(0、0.04、0.16、O.64、1.20mmol/L)染毒16HBE细胞4h,MTT法测定细胞的增殖活性,ELISA法测细胞上清液中Thl、Th2、Thl7类细胞因子和肿瘤坏死因子(TNF-α)的含量。结果与对照组比较,0.32、O.64mmol/L剂量组的细胞存活率下降明显,差异有统计学意义(P〈0.05)。与对照组比较,各染毒组Thl类细胞因子白细胞介素(IL-2)和IL-12含量均降低,干扰素-γ(IFN-γ)、IL-10含量变化不明显;在1.20mmol/L剂量组Th2类细胞因子IL-4含量上升,IL-5、IL-6含量随着染毒剂量的增加呈先上升后下降的趋势,IL_13含量变化不明显;Thl7类细胞因子IL-8含量随着染毒剂量的增加呈先上升后下降的趋势,IL-17含量变化不明显;各染毒组TNF-α含量升高且随着染毒剂量的增加呈上升趋势,其差异均有统计学意义(P〈0.05)。结论甲醛染毒可使人支气管上皮细胞(16HBE细胞)分泌的,Th1,Th2细胞因子比例失衡,IL-8和TNF-α表达升高。
Objective To investigate the effect of formaldehyde exposure on the expression of inflammatory cytokines in human bronchial epithelial cells (16HBE cells). Methods 16HBE cells were treated with formaldehyde with a concentration of 0, 0.04, 0.08, 0.16, 0.32, or 0.64 mmol/L for 24 hours, and MTr assay was applied to measure proliferative activity and calculate median lethal dose; 16HBE ceils were exposed to formaldehyde with a concentration of 0, 0.04, 0.16, 0.64, or 1.20 mmol/L for 4 hours, MTr assay was applied to measure proliferative activity, and enzyme-linked immunosorbent assay was applied to measure the levels of Thl, Th2, and Thl7 cytokines and tumor necrosis factor α (TNF-cx) in cell supernatant. Results Compared with the control group, the 0.32-and 0.64-mmol/L exposure groups had significant decreases in cell viability (P〈0.05); all exposure groups had reductions in interleukin (IL)-2 and IL-12, but no significant changes in interferon-γ and IL-10. In the 1.20-mmol/L exposure group, there was an increase in IL-4, with the increasing exposure dose, IL-5 and IL-6 tended to increase first and then decrease, and there was no significant change in IL-13; with the increasing exposure dose, IL-8 tended to increase first and then decrease, and there was no significant change in IL-17. In all the exposure groups, TNF-α increased and tended to increase significantly with the increasing exposure dose (P〈0.05). Conclusion Formaldehyde exposure can cause imbalance between Thl and Th2 cvtokines secreted by 16HBE ceils, as well as increased expression of IL-8 and TNF-α.