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Note: Autocrine Regulation and Experimental Modulation of Interleukin-6 Expression by Human Pulmonary Epithelial Cells Infected with Respiratory Syncytial Virus

机译:注意:感染呼吸道合胞病毒的人肺上皮细胞的自分泌调节和白细胞介素6表达的实验调节

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摘要

The mechanisms of regulation of interleukin-6 (IL-6) production in respiratory syncytial virus (RSV)-infected respiratory epithelial cells were evaluated in A549 cell cultures. Incubation with purified RSV resulted in significant production of IL-1α, IL-1β, IL-6, and tumor necrosis factor alpha (TNF-α). Addition of saturating concentrations of neutralizing antibodies against IL-1α, IL-1β, or TNF-α into purified RSV-infected cell cultures resulted in a significant inhibition of IL-6 production, although anti-IL-1α antibody had the most predominant effect (80% inhibition). Anti-IL-1α antibody also almost completely blocked the expression of mRNA for IL-6. Addition of therapeutic concentrations of dexamethasone (1 μM) or ribavirin (90 μg/ml), an antiviral agent, also significantly inhibited the synthesis of IL-6. Hence, in clinical settings, pharmacological agents such as the specific antagonists of IL-6-inducing cytokines, as well as dexamethasone and ribavirin, could be used to modulate IL-6 production.
机译:在A549细胞培养物中评估了呼吸道合胞病毒(RSV)感染的呼吸道上皮细胞中白介素6(IL-6)产生的调节机制。用纯化的RSV孵育会大量产生IL-1α,IL-1β,IL-6和肿瘤坏死因子α(TNF-α)。将饱和浓度的针对IL-1α,IL-1β或TNF-α的中和抗体加入纯化的经RSV感染的细胞培养物中可显着抑制IL-6的产生,尽管抗IL-1α抗体的作用最为明显(80%抑制)。抗IL-1α抗体也几乎完全阻断了IL-6 mRNA的表达。添加治疗浓度的地塞米松(1μM)或利巴韦林(90μg/ ml)(一种抗病毒剂)也显着抑制IL-6的合成。因此,在临床环境中,可以使用诸如诱导IL-6的细胞因子的特异性拮抗剂以及地塞米松和利巴韦林的药理剂来调节IL-6的产生。

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