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.
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.
Type
Journal articleSubject
HumansTumor Necrosis Factor-alpha
Intercellular Adhesion Molecule-1
Inflammation Mediators
Interleukin-17
Adolescent
Adult
Middle Aged
Female
Male
Interferon-gamma
Intervertebral Disc Displacement
Intervertebral Disc
Intervertebral Disc Degeneration
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https://hdl.handle.net/10161/18594Published Version (Please cite this version)
10.1002/jor.21206Publication Info
Gabr, 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.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Jun Chen
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.
Robert Douglas Fitch
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
Mostafa Gabr
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&
Lori A. Setton
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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