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Interleukin‐17 synergizes with IFNγ or TNFα to promote inflammatory mediator release and intercellular adhesion molecule‐1 (ICAM‐1) expression in human intervertebral disc cells
Author(s) -
Gabr Mostafa A.,
Jing Liufang,
Helbling Antonia R.,
Sinclair S. Michael,
Allen Kyle D.,
Shamji Mohammed F.,
Richardson William J.,
Fitch Robert D.,
Setton Lori A.,
Chen Jun
Publication year - 2011
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.21206
Subject(s) - mediator , microbiology and biotechnology , intercellular adhesion molecule 1 , adhesion , intercellular adhesion molecule , tumor necrosis factor alpha , intracellular , inflammatory mediator , icam 1 , intervertebral disc , inflammation , chemistry , cell adhesion molecule , cell adhesion , biology , immunology , anatomy , organic chemistry
Interleukin‐17 (IL‐17) is a cytokine recently shown to be elevated, along with interferon‐γ (IFNγ) and tumor necrosis factor (TNFα), 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 IFNγ and TNFα 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, IFNγ, and TNFα. Intervertebral disc cells exposed to IL‐17, IFNγ, or TNFα showed a remarkable increase in inflammatory mediator release and ICAM‐1 expression (GLM and ANOVA, p < 0.05). Addition of IFNγ or TNFα 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 IFNγ and TNFα, 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. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:1–7, 2011