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.
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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.
Tumor Necrosis Factor-alpha
Intercellular Adhesion Molecule-1
Intervertebral Disc Displacement
Intervertebral Disc Degeneration
Published Version (Please cite this version)10.1002/jor.21206
Publication InfoGabr, Mostafa A; Jing, Liufang; Helbling, Antonia R; Sinclair, S Michael; Allen, Kyle D; Shamji, Mohammed F; ... Chen, Jun (2011). 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. Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 29(1). pp. 1-7. 10.1002/jor.21206. Retrieved from https://hdl.handle.net/10161/18594.
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Associate Professor of Orthopaedic Surgery
This author no longer has a Scholars@Duke profile, so the information shown here reflects their Duke status at the time this item was deposited.
Associate Professor of Orthopaedic Surgery
My research interest center around limb lengthening and external fixation. Much is known about the biology of distraction osteogenesis. However, little is known about the effects on the soft tissues with limb lengthening techniques. In a dog model, we are investigating the effects of limb lengthening on muscle function, analizing amount of muscle lengthened per segment of bone lengthening, contractility, and strength. We also hope to begin studies assessing the effects of non steroidal
Research Associate, Senior
Dr. Gabr's research has specifically focused on the following broad areas: (i) animal model of myelopathy, (ii) participating in clinical trials in spine field.In the last few years, this research agenda has expanded to include collaborative projects and publications. Dr. Gabr and his colleagues explore benefit of cervical collar following spine fusion, spinal cord injury model, and transforaminal lumbar interbody fusion.Dr. Gabr is the author of "Interleukin-17 synergizes with IFNI&
Adjunct Professor of Biomedical Engineering
Research in Setton's laboratory is focused on the role of mechanical factors in the degeneration and repair of soft tissues of the musculoskeletal system, including the intervertebral disc, articular cartilage and meniscus. Work in the Laboratory is focused on engineering and evaluating materials for tissue regeneration and drug delivery. Studies combining engineering and biology are also used to determine the role of mechanical factors to promote and control healing of cartilaginous tissues. Re
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