Interleukin-18-induced inflammatory responses in synoviocytes and chondrocytes from osteoarthritic patients
Interleukin-18-induced inflammatory responses in synoviocytes and chondrocytes from osteoarthritic patients
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DOI：
10.3892/ijmm.2012.1073
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发表时间：
2012-10-01
影响因子：
5.4
通讯作者：
Jiang, Jianming
中科院分区：
文献类型：
--
作者：
Fu, Zhaozong;Liu, Peng;Jiang, Jianming
骨关节炎（OA）的主要病理变化包括软骨退变和滑膜炎症。先前的研究证实，白介素-1（IL-1）可刺激滑膜细胞和软骨细胞分泌多种炎症因子。 IL-18 是 IL-1 超家族的成员。在本研究中，研究了 IL-18 对 OA 患者滑膜细胞和软骨细胞的促炎作用。从OA患者身上获取膝关节滑膜和软骨样本，然后培养原代细胞。用IL-18刺激不同代（初级、次级和三级）的滑膜细胞和原代软骨细胞，然后使用逆转录聚合酶链反应（RT-PCR）和酶联免疫吸附测定法测量炎症标志物水平，包括肿瘤坏死因子-α（TNF-α）、前列腺素E-2（PGE（2））和环氧合酶-2（COX-2）。应用IL-1受体拮抗剂(IL-1Ra)干扰IL-18对软骨细胞的刺激，然后测定软骨细胞中COX-2的表达和培养基中PGE的水平。使用 RT-PCR 评估滑膜细胞和软骨细胞中 IL-18 受体 α (IL-18R α) 和 IL-18 受体 β (IL-18R β) 的表达。我们的结果表明，IL-18 刺激原代滑膜细胞中 COX-2 和 TNF-α 的表达，同时增加上清液中 PGE(2) 和 TNF-α 的水平 (P
The major pathological changes of osteoarthritis (OA) include cartilage degeneration and synovial inflammation. Previous studies confirmed that interleukin-1 (IL-1) stimulates the secretion of multiple inflammatory factors in synoviocytes and chondrocytes. IL-18 is a member of the IL-1 superfamily. In this study, the pro-inflammatory effects of IL-18 on synoviocytes and chondrocytes in patients with OA were investigated. Knee synovial membrane and cartilage samples were obtained from OA patients, then primary cells were cultured. Synoviocytes and primary chondrocytes at different generations (primary, secondary and tertiary), were stimulated with IL-18, then inflammatory marker levels, including tumor necrosis factor-alpha (TNF-alpha), prostaglandin E-2 (PGE(2)) and cyclooxygenase-2 (COX-2), were measured using reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay. IL-1 receptor antagonist (IL-1Ra) was applied to interfere with the IL-18 stimulation of chondrocytes, and then the COX-2 expression in chondrocytes and the PGE, levels in the medium were measured. The expression of IL-18 receptor alpha (IL-18R alpha) and IL-18 receptor beta (IL-18R beta) in synoviocytes and chondrocytes was assessed, using RT-PCR. Our results showed that IL-18 stimulated the COX-2 and TNF-alpha expressions in primary synoviocytes, while increasing PGE(2) and TNF-alpha levels in the supernatant (P