Burke J G, G Watson R W, Conhyea D, McCormack D, Dowling F E, Walsh M G, Fitzpatrick J M
Department of Orthopaedic Surgery and Surgical Professorial Unit, Mater Misericordiae Hospital Dublin and University College Dublin, Ireland.
Spine (Phila Pa 1976). 2003 Dec 15;28(24):2685-93. doi: 10.1097/01.BRS.0000103341.45133.F3.
Disc tissue obtained from patients undergoing surgery for scoliosis, lumbar radiculopathy, and discogenic pain was cultured under basal and lipopolysaccharide-stimulated conditions and the medium analyzed for production of a range of pro-inflammatory mediators.
This study was conducted to confirm that the human intervertebral disc is capable of responding to a pro-inflammatory stimulus and to identify the principal mediators involved in any response.
Degenerate human disc tissue has been shown to spontaneously secrete a number of pro-inflammatory mediators. The importance of these molecules in the pathophysiology of symptomatic disc degeneration is increasingly recognized. Human nucleus pulposus has been shown to synthesize increased amounts of interleukin (IL)-6, prostaglandin E2 (PGE2), and nitric oxide in response to stimulation with IL-1beta. Murine nucleus pulposus synthesizes increased amounts of IL-1beta, IL-6, IL-10, and granulocyte-macrophage colony-stimulating factor in response to lipopolysaccharide stimulation. Lipopolysaccharide is a potent inducer of tumor necrosis factor-alpha (TNF-alpha), which is thought to play an important role in the pathophysiology of sciatica. To date, human nucleus pulposus has not been shown to secrete TNF-alpha in response to a pro-inflammatory stimulus.
Human disc tissue obtained from patients undergoing surgery for scoliosis, lumbar radiculopathy, and discogenic pain was cultured under basal and lipopolysaccharide-stimulated conditions and the medium subsequently analyzed for a range of pro-inflammatory mediators.
None of the specimens produced any TNF-alpha, IL-1beta, granulocyte-macrophage colony-stimulating factor, or leukotriene B4. Measurable quantities of IL-6, IL-8, PGE2, MCP-1, basic fibroblast growth factor, and trans forming growth factor-beta1 were produced by a number of specimens. Lipopolysaccharide significantly increased IL-6, IL-8, and PGE2 production in both control and degenerate disc tissue. Degenerate disc specimens responded more vigorously to lipopolysaccharide stimulation than scoliotic specimens.
We conclude that both scoliotic and degenerate human nucleus pulposus can respond to an exogenous pro-inflammatory stimulus by secreting increased amounts of IL-6, IL-8, and PGE2 but not TNF-alpha and that degenerate disc tissue is more sensitive to a pro-inflammatory stimulus than its scoliotic counterpart.
从接受脊柱侧弯、腰椎神经根病和椎间盘源性疼痛手术的患者身上获取椎间盘组织，在基础条件和脂多糖刺激条件下进行培养，并对培养基中一系列促炎介质的产生情况进行分析。
本研究旨在证实人类椎间盘能够对促炎刺激作出反应，并确定参与任何反应的主要介质。
已证明退化的人类椎间盘组织会自发分泌多种促炎介质。这些分子在有症状的椎间盘退变病理生理学中的重要性日益得到认可。已证明人类髓核在受到白细胞介素（IL）-1β刺激时会合成增加量的IL-6、前列腺素E2（PGE2）和一氧化氮。小鼠髓核在受到脂多糖刺激时会合成增加量的IL-1β、IL-6、IL-10和粒细胞-巨噬细胞集落刺激因子。脂多糖是肿瘤坏死因子-α（TNF-α）的强效诱导剂，TNF-α被认为在坐骨神经痛的病理生理学中起重要作用。迄今为止，尚未证明人类髓核在受到促炎刺激时会分泌TNF-α。
从接受脊柱侧弯、腰椎神经根病和椎间盘源性疼痛手术的患者身上获取椎间盘组织，在基础条件和脂多糖刺激条件下进行培养，随后对培养基中一系列促炎介质进行分析。
所有标本均未产生任何TNF-α、IL-1β、粒细胞-巨噬细胞集落刺激因子或白三烯B4。许多标本产生了可测量量的IL-6、IL-8、PGE2、单核细胞趋化蛋白-1、碱性成纤维细胞生长因子和转化生长因子-β1。脂多糖显著增加了对照和退变椎间盘组织中IL-6、IL-8和PGE2的产生。退变椎间盘标本对脂多糖刺激的反应比脊柱侧弯标本更强烈。
我们得出结论，脊柱侧弯和退变的人类髓核均可通过分泌增加量的IL-6、IL-8和PGE2对外部促炎刺激作出反应，但不会分泌TNF-α，并且退变的椎间盘组织比脊柱侧弯的椎间盘组织对促炎刺激更敏感。
