Malaghan Institute of Medical Research, PO Box 7060, Wellington 6242, New Zealand.
Rheumatology (Oxford). 2013 Jun;52(6):1018-21. doi: 10.1093/rheumatology/kes326. Epub 2012 Nov 30.
To investigate the effect of hyperuricaemia on serum chemokine (C-C motif) ligand 2 (CCL2) levels and blood monocytes in people with gout.
Whole blood was collected from subjects with a history of acute or chronic gout but not currently experiencing an attack of gout, subjects with asymptomatic hyperuricaemia and healthy individuals with normouricaemia. Serum concentrations of CCL2 were measured by bead array and levels of CD14(+)/CD11b(+) blood monocytes determined by flow cytometry.
Subjects with gout and asymptomatic hyperuricaemia had higher serum levels of CCL2 and showed an increase in the percentage of circulating CD14(+) monocytes compared with subjects with normouricaemia.
Hyperuricaemia causes elevated serum CCL2 levels and increased monocyte recruitment that may be driven by soluble uric acid-induced CCL2 production. Hyperuricaemia may initiate subclinical priming of circulating blood monocytes for adhesion and trafficking during a gout attack.
探讨高尿酸血症对痛风患者血清趋化因子(C-C 基元)配体 2(CCL2)水平和血单核细胞的影响。
采集有急性或慢性痛风但目前无痛风发作史、无症状高尿酸血症和血尿酸正常者的全血。采用珠阵列法测定血清 CCL2 浓度,流式细胞术测定 CD14(+) / CD11b(+)血单核细胞水平。
痛风和无症状高尿酸血症患者的血清 CCL2 水平较高,与血尿酸正常者相比,循环 CD14(+)单核细胞的百分比增加。
高尿酸血症导致血清 CCL2 水平升高和单核细胞募集增加,这可能是由可溶性尿酸诱导的 CCL2 产生所致。高尿酸血症可能在痛风发作期间引发循环血单核细胞的亚临床预激活,以促进其黏附和迁移。