Study design: 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.
Objectives: To determine the capacity of disc-derived cells to secrete proinflammatory cytokines, and the effect of lipopolysaccharide stimulation on such secretion.
Summary of background data: 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.
Methods: 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.
Results: 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).
Conclusions: 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.