Intervertebral Disc Cells Produce Tumor Necrosis Factor , Interleukin-1, and Monocyte Chemoattractant Protein-1 Immediately After Herniation: An Experimental Study Using a New Hernia Model
Intervertebral Disc Cells Produce Tumor Necrosis Factor , Interleukin-1, and Monocyte Chemoattractant Protein-1 Immediately After Herniation: An Experimental Study Using a New Hernia Model
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DOI：
10.1097/01.brs.0000149194.17891.bf
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发表时间：
2005-01
期刊：
影响因子：
3
通讯作者：
Masakazu Yoshida;Takafumi Nakamura;A. Sei;Taro Kikuchi;K. Takagi;A. Matsukawa
中科院分区：
文献类型：
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作者：
Masakazu Yoshida;Takafumi Nakamura;A. Sei;Taro Kikuchi;K. Takagi;A. Matsukawa
研究设计.在兔中建立了一种新的模拟人类椎间盘突出的疝模型。通过大体外观和组织学检查突出的椎间盘，并研究肿瘤坏死因子、白细胞介素-1和单核细胞趋化蛋白-1的产生。目标.探讨自发性椎间盘突出吸收的早期机制。背景数据总结。突出椎间盘中的巨噬细胞浸润是椎间盘吸收所必需的。然而，手术切除的人类椎间盘突出组织和现有的动物疝模型不适合分析巨噬细胞浸润的机制。最近，我们已经证明，椎间盘细胞能够产生单核细胞趋化蛋白-1，一种有效的巨噬细胞趋化因子，刺激后与肿瘤坏死因子和白细胞介素-1。方法.使用一种新技术在兔子身上手术形成椎间盘突出。手术后在适当的时间间隔切除突出的椎间盘，并检查大小和组织学结果。免疫组化法检测肿瘤坏死因子、白细胞介素-1和单核细胞趋化蛋白-1在突出椎间盘中的表达。结果建立了一种新的兔椎间盘突出模型。术后12周，突出的椎间盘尺寸自发减小。从第3天开始观察到主要由巨噬细胞组成的浸润细胞。免疫组化显示，突出椎间盘中的椎间盘细胞在第1天产生肿瘤坏死因子和白细胞介素-1，随后在第3天产生单核细胞趋化蛋白-1。结论.新的疝模型似乎是非常有用的研究突出的椎间盘吸收。椎间盘细胞可能在椎间盘突出发作后立即产生炎性细胞因子/趋化因子，可能引发随后的巨噬细胞浸润，导致椎间盘吸收。
Study Design. A new hernia model that simulates human disc herniations was developed in rabbits. The herniated discs were examined by gross appearance and histology and production of tumor necrosis factor , interleukin-1, and monocyte chemoattractant protein-1 was investigated. Objectives. To clarify the early mechanism of spontaneous herniated disc resorption. Summary of Background Data. Macrophage infiltration in herniated discs is essential for disc resorption. However, surgically removed human herniated disc tissues and existing animal hernia models are not suitable for analyzing the mechanism of macrophage infiltration. Recently, we have demonstrated that intervertebral disc cells are capable of producing monocyte chemoattractant protein-1, a potent macrophage chemoattractant, after stimulation with tumor necrosis factor and interleukin-1. Methods. Intervertebral disc herniations were surgically developed in rabbits using a new technique. The herniated discs were excised at appropriate time intervals after the surgery, and the size and histologic findings were examined. Expressions of tumor necrosis factor , interleukin-1, and monocyte chemoattractant protein-1 in herniated discs were investigated immunohistochemically. Results. A new rabbit model of disc herniation was established. The herniated discs spontaneously reduced in size by 12 weeks postsurgery. Infiltrating cells, mainly composed of macrophages, were observed from day 3. Immunohistochemically, intervertebral disc cells in the herniated discs produced tumor necrosis factor and interleukin-1 on day 1, followed by monocyte chemoattractant protein-1 on day 3. Conclusions. The new hernia model appears to be very useful for studying herniated disc resorption. Intervertebral disc cells may produce inflammatory cytokines/chemokine immediately after the onset of disc herniation, possibly triggering subsequent macrophage infiltration that leads to disc resorption.