Expression and Distribution of Interleukin-17 in Degenerated Human Cervical Intervertebral Disks

Abstract

IntroductionTo investigate the expression and distribution of interleukin-17 (IL-17) ingenerate human cervical intervertebral disks tissues and to explore the relationship between IL-l7 and cervical intervertebral disk degeneration. Materials and MethodsIL-Iβ,IL-17,tumor necrosis factor (TNF-α), and retinoid-related orphan receptor (RORγt) mRNA levels were respectively measured by real-time quantitative reverse transcription-polymerase chain reaction (QT-PCR) in 30 surgical degenerate cervical intervertebral disk tissues (degeneration group) and 10 nondegenerate control tissues (control group). The level of IL-17 protein and CD4 cell surface antigen were measured by immunohistochemistry staining. ResultsThe mean IL-1β, IL-17, TNF-α, RORγt mRNA levels in degeneration group were significantly higher than that in control group(p < 0.001),and the expression of these factors in nucleus pulposus were significantly higher than that in annulus fibrosus (AF) in degeneration group(p < 0.05). The expression level of IL-17 mRNA was positively correlated with RORγt mRNA level (r = 0.61,p < 0.001). Immunoreactivity of IL-17 and CD4 cell surface antigen were significantly greater in degenerate disks than in controls (p < 0.001),and the immunoreactivity in nucleus pulposus was higher than that in AF in degeneration group(p < 0.05). ConclusionThe expression level of IL-17 mRNA and IL-17 protein were significantly increased in degenerate human cervical disk tissues than that in autopsy control tissues, and the expression in nucleus pulposus was greater than in AF. These findings suggest involvement of IL-17 in the pathomechanism of intervertebral disk degeneration. Immune inflammation mediated by Th17 lymphocytes may play an important role in the development and progression of human cervical intervertebral disk degeneration.I confirm having declared any potential conflict of interest for all authors listed on this abstractYesDisclosure of InterestNone declared