Human Cartilage Homogenates Influence the Crystallization of Monosodium Urate and Inflammatory Response to Monosodium Urate Crystals: A Potential Link Between Osteoarthritis and Gout
Human Cartilage Homogenates Influence the Crystallization of Monosodium Urate and Inflammatory Response to Monosodium Urate Crystals: A Potential Link Between Osteoarthritis and Gout
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DOI：
10.1002/art.41038
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发表时间：
2019-11-06
影响因子：
13.3
通讯作者：
Dalbeth, Nicola
中科院分区：
文献类型：
--
作者：
Chhana, Ashika;Pool, Bregina;Dalbeth, Nicola
目的尿酸钠结晶沉积和痛风发作是骨关节炎关节的常见病变。本研究旨在研究人软骨匀浆对MSU结晶和MSU晶体诱导的炎症的影响。方法从大体上健康和大体上患病的膝关节样品制备人软骨匀浆。结晶测定用于测试软骨匀浆或单个软骨因子对MSU结晶的影响。测定了尿酸盐溶解度、晶体成核、晶体生长和总晶体质量的变化。THP-1细胞测定用于评估在软骨匀浆或单独蛋白存在或不存在下生长的MSU晶体培养后的细胞因子释放。结果与不含软骨匀浆的对照组相比，添加5%或10%健康软骨匀浆增加了形成的MSU晶体的总质量，并导致形成较短的MSU晶体。在存在和不存在软骨匀浆的情况下均观察到MSU晶体弓;然而，在软骨匀浆存在下形成的弓显著短于在其不存在下形成的弓。在所有评估中，肉眼可见健康和肉眼可见病变软骨匀浆之间无效应差异。加入II型胶原或白蛋白也导致形成较短的MSU晶体。在THP-1细胞测定中，与健康软骨匀浆一起生长的MSU晶体增加了白细胞介素-8的释放，而与II型胶原蛋白或白蛋白一起生长的MSU晶体对炎性细胞因子的释放没有影响。结论在尿酸水平升高的情况下，人软骨匀浆增加MSU晶体的形成，并促进具有更大炎症潜能的较小晶体的形成。这些过程可能有助于骨关节炎关节发展痛风的偏好。
Objective Monosodium urate (MSU) crystal deposition and gout flares frequently affect osteoarthritic joints. This study was undertaken to examine the effects of human cartilage homogenates on MSU crystallization and MSU crystal-induced inflammation. Methods Human cartilage homogenates were prepared from macroscopically healthy and macroscopically diseased knee joint samples. Crystallization assays were used to test the effects of cartilage homogenates or individual cartilage factors on MSU crystallization. Changes in urate solubility, crystal nucleation, crystal growth, and total crystal mass were determined. THP-1 cell assays were used to assess cytokine release following culture with MSU crystals grown in the presence or absence of cartilage homogenates or individual proteins. Results Addition of either 5% or 10% healthy cartilage homogenate increased the total mass of MSU crystals formed and resulted in formation of shorter MSU crystals compared to controls without cartilage homogenate. MSU crystal bows were observed in both the presence and absence of cartilage homogenate; however, bows formed in the presence of cartilage homogenates were significantly shorter than bows formed in their absence. There were no effect differences between macroscopically healthy and macroscopically diseased cartilage homogenates in all assessments. Addition of either type II collagen or albumin also led to the formation of shorter MSU crystals. In THP-1 cell assays, MSU crystals grown with healthy cartilage homogenate increased the release of interleukin-8, whereas MSU crystals grown with type II collagen or albumin had no effect on inflammatory cytokine release. Conclusion In the presence of elevated urate levels, human cartilage homogenates increase MSU crystal formation and promote the formation of smaller crystals, which have greater inflammatory potential. These processes may contribute to the predilection of osteoarthritic joints to develop gout.