Interleukin-23 (IL-23, IL-23p19) is a proinflammatory cytokine in the IL-12-related family. Although inflammatory cells in herniated discs have been shown to contain IL-23, little is known about the presence and role of IL-23 in human disc cells. We analyzed disc specimens for IL-23 localization using immunohistochemistry in control, herniated and non-herniated discs from which annulus fibrosus (annulus) cells were isolated and cultured to identify IL-23 gene expression and production. Microarray analysis was used to assess the expression of IL-23 in disc tissue and in cells exposed to two proinflammatory cytokines, IL-1ß and TNF-α. IL-23 was present in annulus cells at the protein level and its expression was up-regulated significantly in herniated compared to control disc tissue. Direct measurement of medium components confirmed production of IL-23 and its receptor, IL-23R, by annulus cells in vitro. Annulus cells in three-dimensional culture exposed to TNF-α, but not IL-1ß, resulted in significant up-regulation of IL-23 expression compared to control cells. Our findings are evidence for the constitutive presence of IL-23 in the human disc and that its expression in vitro is modified by exposure to TNF-α.

中文翻译：

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白细胞介素-23在体内和体外在人环中组成性表达，并在体外被TNF-α上调。

白介素23（IL-23，IL-23p19）是IL-12相关家族中的促炎细胞因子。尽管已显示出椎间盘突出物中的炎性细胞含有IL-23，但对于人椎间盘细胞中IL-23的存在和作用知之甚少。我们使用免疫组织化学分析了椎间盘标本中IL-23的定位，在对照组，椎间盘和非椎间盘中分离了纤维环（环）细胞并进行了培养，以鉴定IL-23基因的表达和产生。微阵列分析用于评估椎间盘组织和暴露于两种促炎细胞因子IL-1ß和TNF-α的细胞中IL-23的表达。IL-23以蛋白质水平存在于环状细胞中，与对照组椎间​​盘组织相比，其在椎间盘突出症中的表达明显上调。对培养基成分的直接测量证实了环空细胞在体外产生IL-23及其受体IL-23R。与对照细胞相比，在三维培养物中暴露于TNF-α而不暴露于IL-1ß的环空细胞导致IL-23表达的显着上调。我们的发现证明了人盘中IL-23的组成性存在，并且其在体外的表达通过暴露于TNF-α而被修饰。