肺炎支原体诱导A549细胞分泌肿瘤坏死因子-α及甲泼尼龙对其的抑制作用

Secretion of Tumor Necrosis Factor-Alpha in A549 Cells Infected with Mycoplasma Pneumoniae and Its Inhibition by Methylprednisolone in Vitro

目的:观察肺炎支原体(Mp)诱导A549细胞产生肿瘤坏死因子-α(TNF-α)及甲泼尼龙(MPL)对TNF-α产生的影响。方法:体外培养A549细胞和MP,用不同感染复数的MP诱导A549细胞,将0.015%的MPL加入到Mp诱导的A549细胞中共同孵育,采用双抗体夹心ELISA法检测不同培养时间的MPL作用于A549细胞后分泌TNF-α的含量。结果:Mp能显著诱导A549细胞分泌TNF-α,其产生水平与Mp刺激时间具有依赖性(r=0.821,P<0.01),当加入0.015%的MPL后,能明显抑制A549细胞分泌TNF-α(P<0.01),且随着Mp感染复数的增加,MPL的抑制作用降低。结论:糖皮质激素(GCs)可抑制MP诱导的A549细胞TNF-α的分泌,提示在MP肺炎时,根据TNF-α的含量变化,适当应用合理剂量的GCs可减轻炎症反应的强度。

Objective： To investigate the effect of tumor necrosis factor-α （TNF-α） production in A549 cells which were induced by Mycoplasma pneumoniae （MP） and to observe the effect on the expression TNF-α protein pretreated with Methylprednisolone （MPL）. Methods： A549 cells and Mp were cultured in vitro. MPL（0. 015%） was administered into culture medium for A549 cells which was pre-induced with Mp of different multiplicity of infection （MOI）. Enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of TNF-α before and after MPL treatment. Results： Mp could significantly induce TNF-α secretion in A549 cells （P〈0.01）. And the level of TNF-α was depended on stimulation time（r=0. 821 ,P〈0.01）. The contents of TNF-α were greatly depressed after 0. 015 MPL treatment （P〈0.01）, but the inhibitory effect of MPL was attenuated with the increasing MOI of Mp. Conclusion： Glucocorticoids （GCs） can obviously inhibit the Mp-induced A549 cells to secrete TNF-α, which suggests that GCs could alleviate the inflammatory response of Mycoplasma Pneumoniae in early stage according to the content of TNF-α.