Role of interleukin-17 in chondrocytes of herniated intervertebral lumbar discs

Lumbar disc herniation (LDH) is a common cause of lumbosacral radiculopathy. An autoimmune response to a herniated nucleus pulposus (NP) has been suggested to play an important role in the initiation of radiculopathy. Interleukin-17 (IL-17) is a cytokine associated with inflammation and autoimmunity. The presence of IL-17 has been studied in patients with LDH; however, extensive investigation into the expression of IL-17 in different disc pathologies of LDH has not yet been conducted. The aim of the present study was to investigate the role of neovascularization and hypertrophic chondrocytes in herniated intervertebral lumbar discs. Fifty-two intervertebral lumbar disc specimens were extracted from 46 patients with LDH and were subsequently classified as either contained or non-contained disc herniation (CDH and NCDH, respectively). The specimens were stained with hematoxylin and eosin or toluidine blue, or were immunostained with polyclonal antibodies to IL-17 using the streptavidin-peroxidase method. The neovascular tissue and staining results were graded to establish the histological differences between the two herniation types. The intervertebral discs (IVDs) obtained from patients with NCDH showed significantly more neovascularization and granulation tissue than the discs obtained from patients with CDH (P<0.05). Furthermore, hypertrophic chondrocytes were more abundant in the NCDH specimens than in the CDH specimens (P<0.05). Similarly, the number of IL-17-immunoreactive cells was significantly higher in the NCDH specimens than that in the CDH specimens (P<0.01). In conclusion, local inflammation and autoreactive immune activation may play an important role in the pathogenesis of LDH. These results also suggest a role of chondrocytes in the repair of herniated IVDs.