IFN-γ and TNF-α induce a different modulation of interleukin-6 in systemic sclerosis fibroblasts compared to healthy controls
IFN-γ and TNF-α induce a different modulation of interleukin-6 in systemic sclerosis fibroblasts compared to healthy controls
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DOI：
10.3109/03009742.2011.585349
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发表时间：
2011-01-01
影响因子：
2.1
通讯作者：
Fallahi, P.
中科院分区：
文献类型：
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作者：
Antonelli, A.;Ferri, C.;Fallahi, P.
背景资料：据我们所知，以前没有研究评估干扰素（IFN）-γ、肿瘤坏死因子（TNF）-α或它们的组合对系统性硬化症（SSc）患者在疾病早期的原代培养成纤维细胞中原型促炎细胞因子白细胞介素（IL）-6的影响。五名SSc患者的成纤维细胞培养物评估了（疾病持续时间< 2年）和五名健康对照者单独或联合使用TNF-α或IFN-γ刺激后IL-6的基础产生。结果：在基础条件下，来自SSc患者的成纤维细胞产生比对照更高水平的IL-6 [ 617 +/-173对213 +/-123 pg/mL;方差分析（ANOVA），p < 0.001]。TNF-α能够在SSc中剂量依赖性地诱导IL-6（分别为609 +/-184，723 +/-243，1079 +/-297，1436 +/-326 pg/mL，TNF-α为0、1、5、10 ng/mL），但在对照成纤维细胞中不能，而IFN-γ不能诱导IL-6。此外，IFN-γ和TNF-α的组合在SSc成纤维细胞中诱导更强的IL-6分泌（ANOVA，p < 0.0001），而在对照中没有影响。
Background: To our knowledge, no previous study has evaluated the effect of interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha, or their combination on the prototype proinflammatory cytokine interleukin (IL)-6 in primary cultured fibroblasts from patients with systemic sclerosis (SSc) at an early stage of the disease.Methods: Fibroblast cultures from five SSc patients (disease duration < 2 years) and five healthy controls were evaluated for the basal production of IL-6, and after stimulation with TNF-alpha or IFN-gamma, alone or combined.Results: The fibroblasts from SSc patients produced higher levels of IL-6 in basal condition than controls [ 617 +/- 173 vs. 213 +/- 123 pg/mL; analysis of variance (ANOVA), p < 0.001]. TNF-a was able to dose-dependently induce IL-6 in SSc (609 +/- 184, 723 +/- 243, 1079 +/- 297, 1436 +/- 326 pg/mL, with TNF-a 0, 1, 5, 10 ng/mL, respectively) but not in control fibroblasts, whereas IFN-gamma was unable to induce IL-6. Furthermore, the combination of IFN-gamma and TNF-a induced a stronger secretion of IL-6 in SSc fibroblasts (ANOVA, p < 0.0001), without effect in controls.Conclusions: SSc fibroblasts participate in the self-perpetuation of inflammation by releasing IL-6, under the influence of TNF-alpha and/or IFN-gamma.