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.
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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DOI：
10.1002/jor.21206
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发表时间：
2011-01
影响因子：
2.8
通讯作者：
Chen, Jun
中科院分区：
文献类型：
--
作者：
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
白细胞介素-17（IL-17）是一种细胞因子，最近显示在退变和突出的椎间盘（IVD）组织中与干扰素-γ（IFNγ）和肿瘤坏死因子（TNFα）沿着升高，表明这些细胞因子在椎间盘疾病中的作用。本研究的目的是探讨IL-17和共刺激因子IFNγ和TNFα在椎间盘病理学中的作用。从进行椎间盘变性或脊柱侧凸手术的患者的纤维环和髓核组织中分离细胞。在暴露于IL-17、IFNγ和TNFα后，对培养细胞的炎症介质、一氧化氮（NOx）、前列腺素E2（PGE 2）和白细胞介素-6（IL-6）的产生以及细胞间粘附分子（ICAM-1）的表达进行定量。IL-17、IFN-γ和TNF-α处理的椎间盘细胞炎性介质释放和ICAM-1表达均显著增加（GLM和ANOVA，p<0.05）。在IL-17中加入IFNγ或TNFα可协同增加炎症介质的释放，并显著增加ICAM-1的表达。这些结果表明，IVD细胞不仅对IL-17和共刺激因子IFNγ和TNFα产生分解代谢表型反应，而且还表达表面配体，从而有可能招募额外的淋巴细胞和免疫细胞进入IVD微环境。IL-17可能是IVD病理学中炎症的重要调节剂。
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.
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影响因子：
4.6
作者：
Katz, Y;Nadiv, O;Loos, M
通讯作者：
Loos, M
影响因子：
100.3
作者：
Dong, C
通讯作者：
Dong, C
影响因子：
3.8
作者：
Chabaud, M;Garnero, P;Miossec, P
通讯作者：
Miossec, P
影响因子：
4.4
作者：
HELIOVAARA, M;SIEVERS, K;AROMAA, A
通讯作者：
AROMAA, A
DOI：
10.1084/jem.183.6.2593
发表时间：
1996-06-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Fossiez F;Djossou O;Chomarat P;Flores-Romo L;Ait-Yahia S;Maat C;Pin JJ;Garrone P;Garcia E;Saeland S;Blanchard D;Gaillard C;Das Mahapatra B;Rouvier E;Golstein P;Banchereau J;Lebecque S
通讯作者：
Lebecque S