Abstract
Objective and Background: Interleukin 1 has been implicated in the progression of degenerative disc disease, however little data is available on the expression and production of IL-1 within degenerate discal cells. A few studies, have investigated herniated disc tissue but the results from these studies have been inconsistent. This study investigated the gene expression of IL-1 α, β, Ra and the receptor type I in discs removed at surgery from 7 prolapsed, 3 Scoliosis and 15 Degenerative discs (DD). In addition immunohistochemistry (IHC) was used to localise IL-1 α and IL-1 β within normal, and degenerate discs.
Methods: Human IVD tissue was obtained from disc replacement surgery and separated into nucleus pulposus (NP) and annulus fibrosus (AF) tissue, cell isolation using collagenase treatment was carried out, and RNA extraction on the cells performed immediately. Real time RT-PCR was then used to investigate gene expression of IL-1 gene family. IHC for IL-1 α and IL-1 β was also performed on paraffin embedded normal and degenerate disc samples.
Results: Expression of the IL-1 family genes was present at low levels within prolapsed disc samples. In contrast levels within scoliosis patents were the highest of the 3 disease states, however in both prolapsed discs and those from scoliosis patients a balance of IL-1 α/β to IL-1 Ra existed. Within samples from DD this balance was lost, with levels of IL-1 α and IL-1 β greatly exceeding levels of IL-1 Ra. In addition levels of IL-1 α and β showed an increase with age and were highest in those samples from the AF than the NP. IHC demonstrated both IL-1 α and IL-1 β protein within the NP and AF cells of the degenerate discs.
Conclusion: This study has demonstrated the mRNA expression of all members of the IL-1 family within IVD and in addition the chondrocytes within the disc produced IL-1 α and IL-1 β protein. The imbalance of IL-1 α/β to IL-1 Ra within those samples from degenerate discs but not prolapsed or scoliotic discs suggests a role for IL-1 within discal degeneration.
Correspondence should be addressed to the editorial secretary: Dr Charles Pither, c/o British Orthopaedic Society, Royal College of Surgeons, 35-43 Lincoln’s Inn Fields, London WC2A 3PN.
