Gómez-Chiarri M, Hamilton T A, Egido J, Emancipator S N
Renal Unit, Fundación Jiménez Díaz, Madrid, Spain.
Am J Pathol. 1993 Feb;142(2):433-9.
IP-10 is an early gene induced in multiple cell types by a variety of proinflammatory agents, notably interferons (IFNs) and lipopolysaccharide (LPS). To determine whether this protein might play a role in amplifying immune-mediated glomerular injury, we cultured mouse mesangial cells with several stimuli for various times. Increasing amounts of IFN-gamma (to 100 units/ml) elicited increasing levels of IP-10 messenger RNA (mRNA), sustained to 24 hours, but had no effect on tumor necrosis factor-alpha (TNF-alpha) mRNA. LPS induced transient IP-10 mRNA expression that peaked at 8 hours; TNF-alpha mRNA was also increased. TNF-alpha at doses up to 10 ng/ml and soluble immune complexes up to 150 micrograms/ml antibody evoked 3- to 5-fold increases in IP-10 mRNA expression, much less than the 30- to 70-fold increases seen with IFN-gamma and LPS. We conclude that IFN-gamma, LPS, and other agonists can amplify glomerular immune injury, perhaps via elevated expression of IP-10.
IP - 10是一种早期基因，可被多种促炎因子诱导在多种细胞类型中表达，尤其是干扰素（IFN）和脂多糖（LPS）。为了确定该蛋白是否可能在放大免疫介导的肾小球损伤中发挥作用，我们用几种刺激物对小鼠系膜细胞进行了不同时间的培养。增加干扰素 - γ的量（至100单位/毫升）会使IP - 10信使核糖核酸（mRNA）水平不断升高，并持续至24小时，但对肿瘤坏死因子 - α（TNF - α）mRNA没有影响。LPS诱导IP - 10 mRNA短暂表达，在8小时达到峰值；TNF - α mRNA也增加。剂量高达10纳克/毫升的TNF - α和抗体浓度高达150微克/毫升的可溶性免疫复合物可使IP - 10 mRNA表达增加3至5倍，远低于干扰素 - γ和LPS所引起的30至70倍的增加。我们得出结论，干扰素 - γ、LPS和其他激动剂可能通过升高IP - 10的表达来放大肾小球免疫损伤。
