Tilg H, Vogel W, Dinarello C A
Department of Medicine, University Hospital Innsbruck, Austria.
Blood. 1995 Jan 15;85(2):433-5.
In the present studies we investigated the effect of interferon-alpha (IFN alpha) on the release of the soluble (extracellular) form of the tumor necrosis factor p55 receptor (TNFsRp55), because TNFsRp55 is a natural antagonist of tumor necrosis factor (TNF)-induced inflammation and also might be part of the antiinflammatory properties of IFN alpha. Plasma levels of TNFsRp55 were measured by a specific radioimmunoassay in five healthy volunteers and in five patients with chronic hepatitis C treated with IFN alpha. Levels showed a significant increase after a single injection of 5.0 million U IFN alpha in both healthy and hepatitis patient groups. Peak values (3.5 to 4.5 ng/mL) were observed within 12 hours of beginning treatment. Thereafter, levels promptly declined, reaching baseline values within 24 hours. TNF alpha and C-reactive protein (CRP) levels were below the detection limit in the same plasma samples. In addition, IFN alpha suppressed significantly interleukin (IL)-1 alpha-induced TNF alpha protein synthesis by human peripheral blood mononuclear cells. These results suggest that the antiinflammatory properties of IFN alpha may be, in part, also due to the induction and/or release of TNF soluble receptors and the suppression of TNF alpha synthesis.
在本研究中，我们探究了α干扰素（IFNα）对肿瘤坏死因子p55受体可溶性（细胞外）形式（TNFsRp55）释放的影响，因为TNFsRp55是肿瘤坏死因子（TNF）诱导炎症的天然拮抗剂，也可能是IFNα抗炎特性的一部分。通过特异性放射免疫分析法测定了5名健康志愿者和5名接受IFNα治疗的慢性丙型肝炎患者血浆中TNFsRp55的水平。在健康组和肝炎患者组中，单次注射500万单位IFNα后，水平均显著升高。在开始治疗后的12小时内观察到峰值（3.5至4.5 ng/mL）。此后，水平迅速下降，在24小时内恢复到基线值。在相同的血浆样本中，TNFα和C反应蛋白（CRP）水平低于检测限。此外，IFNα显著抑制人外周血单核细胞中白细胞介素（IL）-1α诱导的TNFα蛋白合成。这些结果表明，IFNα的抗炎特性可能部分也归因于TNF可溶性受体的诱导和/或释放以及TNFα合成的抑制。
