Role of cytokines in intervertebral disc degeneration: pain and disc content.
Role of cytokines in intervertebral disc degeneration: pain and disc content.
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DOI：
10.1038/nrrheum.2013.160
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发表时间：
2014-01
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影响因子：
--
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中科院分区：
文献类型：
--
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椎间盘退变是背部/颈部和神经根疼痛的主要原因。其特征在于椎间盘细胞自身分泌的炎性细胞因子肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1 α/β、IL-6和IL-17水平升高;这些细胞因子促进基质降解、趋化因子产生和细胞表型变化。由此产生的分解代谢和合成代谢反应之间的不平衡导致变性，以及疝和神经根疼痛。趋化因子从退变椎间盘的释放促进T和B细胞、巨噬细胞、嗜中性粒细胞和肥大细胞的浸润和活化，进一步放大炎症级联反应。免疫细胞迁移到椎间盘中伴随着从背根神经节（DRG）产生的微血管和神经纤维的出现。在这种炎症环境中，由椎间盘和免疫细胞产生的神经原性因子，特别是神经生长因子（NGF）和脑源性神经营养因子（BDNF）诱导DRG中疼痛相关阳离子通道的表达。这些通道的去极化可能会促进椎间盘源性和神经根性疼痛，并加强细胞因子介导的退行性级联反应。总之，对细胞因子和免疫细胞在分解代谢和伤害感受过程中的作用的进一步理解为治疗症状性椎间盘疾病提供了新的靶点。
Degeneration of the intervertebral disc is the major contributor to back/neck and radicular pain. It is characterized by an elevation in levels of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1 α/β, IL-6 and IL-17 secreted by the disc cells themselves; these cytokines promote matrix degradation, chemokine production and changes in cell phenotype. The resulting imbalance between catabolic and anabolic responses leads to degeneration, as well as herniation and radicular pain. Release of chemokines from degenerating discs promote infiltration and activation of T and B cells, macrophages, neutrophils, and mast cells further amplifying the inflammatory cascade. Immunocyte migration into the disc is accompanied by the appearance of microvasculature and nerve fibers arising from the dorsal root ganglion (DRG). In this inflammatory milieu, neurogenic factors in particular nerve growth factor (NGF) and brain-derive neurotrophic factor (BDNF) generated by disc and immune cells induce expression of pain associated cation channels in DRGs. Depolarization of these channels is likely to promote discogenic and radicular pain and reinforce the cytokine-mediated degenerative cascade. Taken together, the enhanced understanding of the contribution of cytokines and immune cells to catabolic and nociceptive processes provide new targets for treating symptomatic disc disease.
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