Immune cell infiltration and inflammatory response in nucleus pulposus following annular disruption in degenerative disc disease

Intervertebral disc degeneration (IDD) is a common cause of lower back pain. However, the role of annulus fibrosus rupture in altering the immune microenvironment of nucleus pulposus remains unclear. This study elucidated the impact of annulus fibrosus rupture on the immune response within the nucleus pulposus in IDD. The study included patients diagnosed with intervertebral disc herniation who underwent surgical treatment at the Orthopedics Department of the Second Hospital of Soochow University from September 2020 to July 2021. Based on the integrity of the annulus fibrosus, patients were categorized into two groups: Annulus Intact (AI) group and Annulus Rupture (AR) group. Nucleus pulposus samples were collected during surgery for analysis. Flow cytometry was used to assess immune cell populations in these samples. Levels of inflammatory factors were measured using RT-PCR and enzyme-linked immunosorbent assay (ELISA). Samples from patients with annulus rupture showed significantly higher levels of macrophages and T cells compared to those with intact annulus. Gene expression of key inflammatory cytokines, including TNF-α, IL-1β, IL-4, and IL-6, were markedly elevated in the AR group than those in AI group (P < 0.05). The levels of TNF-α and IL-1β detected by ELISA were also significantly increased in AR group (P < 0.05). Annulus fibrosus rupture significantly alters the immune microenvironment of the nucleus pulposus, characterized by increased inflammatory cell infiltration and elevated levels of pro-inflammatory cytokines. This enhanced local inflammatory response may play a crucial role in the pathogenesis and progression of IDD, offering potential targets for immune-modulatory therapies to delay IDD progression.