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dc.contributor.author Gabr, Mostafa A.
dc.contributor.author Jing, Liufang
dc.contributor.author Helbling, Antonia R.
dc.contributor.author Sinclair, S. Michael
dc.contributor.author Allen, Kyle D.
dc.contributor.author Shamji, Mohammed F.
dc.contributor.author Richardson, William
dc.contributor.author Fitch, Robert
dc.contributor.author Setton, Lori A.
dc.contributor.author Chen, Jun
dc.date.accessioned 2011-01-19T17:42:09Z
dc.date.available 2011-01-19T17:42:09Z
dc.date.issued 2011-01-01
dc.identifier.citation Journal of Orthopaedic Research, Volume 29, Issue 1, pages 1–7, January 2011 en_US
dc.identifier.uri http://hdl.handle.net/10161/3167
dc.description.abstract 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. en_US
dc.description.sponsorship Supported by grants from the NIH R01AR047442, P01AR05024506, R01AR057410, R01EB00226307, K99AR057426 and NCBC GRANT #2008-CFG-8013. This study was also supported by the Pratt Undergraduate Research Fellowship and the Howard Clark Pre-Doctoral Fellowship. en_US
dc.language.iso en_US en_US
dc.publisher Wiley Press en_US
dc.relation.ispartofseries Journal of Orthopaedic Reserach;
dc.relation.isversionof DOI: 10.1002/jor.2120 en_US
dc.subject intervertebral disc, cytokine, inflammation, interleukin-17, ICAM-1 en_US
dc.title 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 en_US
dc.type Article en_US

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