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

Abstract

Abstract. 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.

<p>Characterization of novel lnc RNAs in the spinal cord of rats with lumbar disc herniation</p>

“…In recent years, the underlying molecular mechanisms of radicular pain have been widely studied; however, the epigenetic process of pain is still unclear 25. lncRNAs have complicated molecular functions, including regulating protein activities, serving structural or organizational roles, serving as precursors to small RNAs, modulating transcriptional patterns, and altering RNA-processing events 26. The function of lncRNAs in regulating the gene expression of neuropathic pain is unclear.…”

Exploratory study for identifying systemic biomarkers that correlate with pain response in patients with intervertebral disc disorders

“…In DH, IL-17 has been proposed as a potential player in the pathomechanism of degeneration, with a potentially greater contribution from infiltrating inflammatory cells than disc cells [ 39 – 41 ]. Herniation severity may also modulate the relative contribution of IL-17 in DH, with greater IL-17 immunoreactive cells found in ruptured DH specimens than specimens contained within the disc boundary [ 42 ]. We did not evaluate changes in mediator levels based on severity of herniation, though our findings of decreased IL-17 levels in DH subjects post-ESI treatment supports the evidence for its potential role in the pathomechanism.…”

Network Pharmacological Dissection of the Mechanisms of Eucommiae Cortex-Achyranthis Radix Combination for Intervertebral Disc Herniation Treatment

“…142 The autoimmunity- and inflammation-associated interleukin (IL)-17 pathway acts as a key mediator of IVD deterioration and IDH progression, and its higher activity is observed in the IVD tissues of patients with IDH. 143,144 Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway acts as an inflammation regulator and causes IDH-associated symptoms that are important for the degeneration of herniated IVDs. 145 The migration and infiltration of leukocytes into IVD tissues, accompanied by angiogenesis, neovascularization, and appearance of nerve fibers, may accelerate the inflammatory IVD degeneration and IDH-related disease processes.…”