mRNA expression of cytokines and chemokines in herniated lumbar intervertebral discs

Study Design. The mRNA expressions of cytokines and chemokines were assessed in herniated lumbar disc specimens. Objectives. To investigate whether the mRNAs of interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, RANTES, IL-8, IL-10, and transforming growth factor (TGF)-beta are expressed in surgically obtained herniated disc specimens; and to discover which of them are the predominant cytokines associated with the clinical symptoms and signs, and whether any differences in the mRNA expression exist depending on the different types of disc herniations. Summary of Background Data. It has been postulated that cytokines are involved in causing radicular leg pain in lumbar disc herniations. Although a few studies have been done on lumbar disc herniations concerning IL-1alpha and TNF-alpha, almost none has been carried out in the cases of the other of cytokines and chemokines. Methods. Using a reverse transcription-polymerase chain reaction, mRNA expressions of cytokines and chemokines were investigated in herniated disc specimens. The straight leg raising test, development of radicular pain by back extension, symptom duration, pain intensity using a visual analogue scale, and herniation types were described. Results. The mRNAs of IL-8, TNF-alpha, IL-1alpha, RANTES, and IL-10 were expressed in 16 (70%), 15 (65%), 9 (39%), 4 (17%), and 2 (9%) of the 23 herniated disc specimens, respectively. The mRNA of TGF-beta was expressed in 5 of 10 specimens (50%). IL-8 mRNA expression was associated with the development of radicular pain by back extension and short symptom duration (average 3.8 weeks). The mRNAs of IL-1alpha were expressed more frequently in transligamentous extensions than in subligamentous extensions, but the expression was weak. Conclusion. Interleukin-8 appears to be associated with development of radicular pain by back extension and to be activated on acute or subacute disc herniations. IL-8 seems to participate in the pathomechanism of nerve root inflammation in lumbar disc herniations, which implies that it may be considered a target for therapeutic intervention.