Abstract

We sought to determine whether high-density lipoprotein (HDL) function was altered in gout patients. The study included 95 gout patients and 68 healthy controls. The concentrations of interleukin (IL)-1β and IL-9 were measured by ELISA, and indicators such as blood uric acid, liver and kidney function, blood glucose, and blood lipids were detected. To test for the anti-inflammatory and reverse cholesterol transport (RCT) function of HDL, 11 gout patients and 11 healthy controls were randomly selected for the BioVision cholesterol efflux test, which detects the RCT activity of HDL. To assess the anti-inflammatory function of HDL, cells in co-culture with HDL were treated with inflammatory stimuli such as tumor necrosis factor-α (TNF-α), and then, the cells were assayed for the expression of intercellular adhesion molecules (ICAMs) and vascular cell adhesion molecule-1 (VCAM-1). In total, this study enrolled 163 participants, including 95 non-hyperlipidemic gout patients and 68 healthy controls. IL-1β and IL-9 levels were significantly higher in the gout group than in the control group (85.26 ± 23.16 vs. 41.47 ± 6.48 and 33.77 ± 12.68 vs. 23.66 ± 4.53, respectively, P < 0.001). Additionally, plasma IL-1β and IL-9 levels were increased along with those of blood uric acid (R2 = 0.4116 and R2 = 0.4150, respectively, P < 0.001). Compared with the healthy controls, gout patients showed no differences in plasma apoA-1 levels or in the cholesterol efflux assay. Gout patients had increased ICAM-1 expression compared with the healthy controls (88.79 ± 3.68 vs. 86.27 ± 4.64, P < 0.05), but no difference in VCAM-1 expression was found (0.87 ± 0.43 vs. 0.98 ± 0.96, P > 0.05). In this assay, higher values indicate less suppression of ICAM-1 induction, which correlates with a reduced anti-inflammatory capacity. The anti-inflammatory activities of HDLs are impaired in gout patients. Key Points • Gout patients show chronic inflammation. • The anti-inflammatory activity of high-density lipoprotein is impaired in gout patients.

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