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目的:观察肺炎支原体(Mp)体外诱导A549细胞(人肺腺癌上皮细胞株)产生肿瘤坏死因子-α(TNF-α)的水平以及血管活性肠肽(VIP)对TNF-α产生水平的影响。方法:将A549细胞与不同感染复数和不同刺激时间的Mp共同孵育,用ELISA法检测细胞培养上清液中TNF-α的含量;用不同浓度的VIP预处理A549细胞,然后再以Mp诱导,测定细胞培养上清液中TNF-α的含量。结果:A549细胞经Mp刺激后,TNF-α的产生水平明显高于正常细胞对照组(P<0.05),且TNF-α的产生水平与Mp的感染复数和感染时间具有依赖性。VIP不同浓度的干预,A549细胞TNF-α的分泌浓度较无VIP干预组有不同程度的降低(P<0.05)。结论:Mp可诱导A549细胞产生TNF-α,VIP可有效降低Mp诱导的TNF-α的产生,提示VIP对肺上皮细胞有直接抗炎作用。
Objective: To investigate the effect of Mycoplasma pneumoniae (Mp) on the level of tumor necrosis factor-α (TNF-α) and the production of TNF-α in A549 cells (human lung adenocarcinoma cell line) in vitro . Methods: A549 cells were incubated with Mp with different numbers of infection and different stimulation time. The content of TNF-α in cell culture supernatant was detected by ELISA. A549 cells were pretreated with different concentrations of VIP and then induced by Mp. The content of TNF-α in the cell culture supernatant was measured. Results: After stimulated with Mp, the level of TNF-α in A549 cells was significantly higher than that in normal cells (P <0.05). The production level of TNF-α was dependent on the multiplicity of infection and the time of infection. In different concentrations of VIP, the secretion of TNF-α in A549 cells was lower than that in the non-VIP intervention group (P <0.05). Conclusion: Mp can induce TNF-α production in A549 cells. VIP can effectively reduce Mp-induced TNF-α production, suggesting that VIP has a direct anti-inflammatory effect on lung epithelial cells.