Aspirin-induced increases in soluble IL-1 receptor type II concentrations in vitro and in vivo

This study examined the influence of low-dose aspirin on interleukin (IL)-1 beta, IL-1 receptor antagonist (IL-1ra), and soluble receptor type II (sIL-1RII) secretion in vivo and in vitro. Blood mononuclear cells were isolated from healthy young men who ingested 81 mg of aspirin on alternate days for 2 weeks and from unmedicated controls. Aspirin had minor effects on ex vivo secretion of IL-1 beta and no influence on IL-1ra. In contrast, unstimulated ex vivo secretion of sIL-1RII was over twice as high by cells front aspirin-treated subjects (1115 +/- 123 vs, 460 +/- 77 pg/mL, P = 0.02), Lipopolysaccharide-stimulated sIL-1RII secretion was influenced similarly. Plasma sIL-1RII concentrations were 23% higher in aspirin-treated subjects (10.2 +/- 0.6 vs. 8.4 +/- 0.3 ng/mL, P = 0.03), In addition, cells from unmedicated subjects cultured in, vitro with aspirin (10 mu g/mL) secreted significantly greater amounts of sIL-1RII. Thus, low-dose aspirin therapy may prevent inflammation by increasing soluble receptor secretion, thereby preventing IL-1 from binding target cells.