Interleukin-17 synergizes with IFN? or TNFa to promote inflammatory mediator release and intercellular adhesion molecule-1 (ICAM-1) expression in human intervertebral disc cells.

Gabr MA, Jing L, Helbling AR, Sinclair SM, Allen KD, Shamji MF, Richardson WJ, Fitch RD, Setton LA, Chen J. Interleukin-17 synergizes with IFN? or TNFa to promote inflammatory mediator release and intercellular adhesion molecule-1 (ICAM-1) expression in human intervertebral disc cells. Journal of orthopaedic research : official publication of the Orthopaedic Research Society. 2011 Jan 1; 29(1):1-7.

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Abstract:

Interleukin-17 (IL-17) is a cytokine recently shown to be elevated, along with interferon- (IFN ) and tumor necrosis factor (TNF ), in degenerated and herniated intervertebral disc (IVD) tissues, suggesting a role for these cytokines in intervertebral disc disease. The objective of our study was to investigate the involvement of IL-17 and costimulants IFN and TNF in intervertebral disc pathology. Cells were isolated from anulus fibrosus and nucleus pulposus tissues of patients undergoing surgery for intervertebral disc degeneration or scoliosis. The production of inflammatory mediators, nitric oxide (NOx), prostaglandin E2 (PGE2) and interleukin-6 (IL-6), as well as intercellular adhesion molecule (ICAM-1) expression, were quantified for cultured cells following exposure to IL-17, IFN , and TNF . Intervertebral disc cells exposed to IL-17, IFN , or TNF showed a remarkable increase in inflammatory mediator release and ICAM-1 expression (GLM and ANOVA, p < 0.05). Addition of IFN or TNF to IL-17 demonstrated a synergistic increase in inflammatory mediator release, and a marked increase in ICAM-1 expression. These findings suggest that IVD cells not only respond with a catabolic phenotype to IL-17 and costimulants IFN and TNF , but also express surface ligands with consequent potential to recruit additional lymphocytes and immune cells to the IVD microenvironment. IL-17 may be an important regulator of inflammation in the IVD pathologies.