University of Auckland, Auckland, New Zealand.
Auckland City Hospital, Auckland, New Zealand.
Arthritis Rheumatol. 2019 Dec;71(12):2090-2099. doi: 10.1002/art.41038. Epub 2019 Nov 6.
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.
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.
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.
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.
尿酸单钠（MSU）晶体沉积和痛风发作常影响骨关节炎关节。本研究旨在研究人软骨匀浆对 MSU 结晶和 MSU 晶体诱导炎症的影响。
从宏观上健康和患有膝关节疾病的膝关节样本中制备人软骨匀浆。结晶测定法用于测试软骨匀浆或个别软骨因子对 MSU 结晶的影响。测定尿酸溶解度、晶体成核、晶体生长和总晶体质量的变化。使用 THP-1 细胞测定法，在存在或不存在软骨匀浆或个别蛋白质的情况下，培养 MSU 晶体后，评估细胞因子的释放。
添加 5%或 10%健康软骨匀浆会增加形成的 MSU 晶体总质量，并导致与无软骨匀浆的对照相比形成更短的 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，但在存在软骨匀浆的情况下形成的弓明显短于不存在软骨匀浆的弓。在所有评估中，宏观上健康和患有膝关节疾病的软骨匀浆之间没有差异。添加 II 型胶原或白蛋白也导致形成更短的 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 型胶原或白蛋白一起生长的 MSU 晶体对炎症细胞因子的释放没有影响。
在尿酸水平升高的情况下，人软骨匀浆增加 MSU 晶体形成并促进较小晶体的形成，从而具有更大的炎症潜力。这些过程可能导致骨关节炎关节易发生痛风。
