Rand N, Reichert F, Floman Y, Rotshenker S
Vanderbilt University Spine Center, Nashville, Tennessee 37232-2550, USA.
Spine (Phila Pa 1976). 1997 Nov 15;22(22):2598-601; discussion 2602. doi: 10.1097/00007632-199711150-00002.
Cultures established from murine disc-derived cells were stimulated by lipopolysaccharide. The cells' capacity to secrete proinflammatory cytokines and interleukin-10 with and without lipopolysaccharide stimulation was determined using enzyme-linked immunosorbent assays.
To determine the capacity of disc-derived cells to secrete proinflammatory cytokines, and the effect of lipopolysaccharide stimulation on such secretion.
The pathophysiology of compressive radiculopathy is unclear. Inflammation is a possible explanation. Proinflammatory cytokine secretion was demonstrated in herniated nucleus pulposus. It is unknown whether these cytokines are secreted from disc-derived cells or from infiltrating inflammatory cells in the herniated nucleus pulposus.
Discs were microsurgically harvested from inbred mice and cut to allow the nucleus pulposus to establish cell culture. A study group was exposed to lipopolysaccharide stimulation. Media were harvested from the study and control groups 24 hours later. Secretion of interleukins-1-, -6, and -10, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-alpha were determined using enzyme-linked immunosorbent assays.
Basal secretion of interleukins-6 and -10, but no basal secretion of interleukin-1-, granulocyte-macrophage colony-stimulating factor, or tumor necrosis factor-alpha was detected. Secretion of interleukin-1- rose from zero to 27.69 pg/10(5) cells, and granulocyte-macrophage colony-stimulating factor secretion rose from zero to 9.77 pg/10(5) cells after lipopolysaccharide stimulation. A 75-fold increase in interleukin-6 secretion and a 150-fold increase in interleukin-10 secretion were detected after stimulation with lipopolysaccharide. No tumor necrosis factor-alpha secretion was detectable. All result had high statistical significance (all P < 0.001).
Cultured murine disc-derived cells have the capacity to secrete proinflammatory cytokines and interleukin-10 in the absence of inflammatory cells. This finding supports the hypothesis that disc-derived cells are capable of initiating or amplifying an inflammatory process.
用脂多糖刺激从小鼠椎间盘来源细胞建立的培养物。使用酶联免疫吸附测定法测定细胞在有和没有脂多糖刺激的情况下分泌促炎细胞因子和白细胞介素-10的能力。
确定椎间盘来源细胞分泌促炎细胞因子的能力,以及脂多糖刺激对这种分泌的影响。
压迫性神经根病的病理生理学尚不清楚。炎症是一种可能的解释。在突出的髓核中已证实有促炎细胞因子分泌。尚不清楚这些细胞因子是由椎间盘来源的细胞分泌的,还是由突出髓核中浸润的炎性细胞分泌的。
通过显微手术从近交系小鼠中获取椎间盘并进行切割,以使髓核建立细胞培养。一个研究组接受脂多糖刺激。24小时后从研究组和对照组收集培养基。使用酶联免疫吸附测定法测定白细胞介素-1、-6和-10、粒细胞巨噬细胞集落刺激因子以及肿瘤坏死因子-α的分泌。
检测到白细胞介素-6和-10的基础分泌,但未检测到白细胞介素-1、粒细胞巨噬细胞集落刺激因子或肿瘤坏死因子-α的基础分泌。脂多糖刺激后,白细胞介素-1的分泌从零增加到27.69 pg/10(5)细胞,粒细胞巨噬细胞集落刺激因子的分泌从零增加到9.77 pg/10(5)细胞。脂多糖刺激后,白细胞介素-6的分泌增加了75倍,白细胞介素-10的分泌增加了150倍。未检测到肿瘤坏死因子-α的分泌。所有结果均具有高度统计学意义(所有P < 0.001)。
培养的小鼠椎间盘来源细胞在没有炎性细胞的情况下有分泌促炎细胞因子和白细胞介素-10的能力。这一发现支持了椎间盘来源细胞能够启动或放大炎症过程的假说。