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Aspirin‐induced increases in soluble IL‐1 receptor type II concentrations in vitro and in vivo
Author(s) -
Daun Jane M.,
Ball Richard W.,
Burger Heather R.,
Can Joseph G.
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.65.6.863
Subject(s) - in vivo , biology , in vitro , aspirin , pharmacology , receptor , immunology , biochemistry , microbiology and biotechnology
This study examined the influence of low‐dose aspirin on interleukin (IL)‐1β, 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‐1β and no influence on IL‐1ra. In contrast, unstimulated ex vivo secretion of sIL‐1RII was over twice as high by cells from 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 μg/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. J. Leukoc. Biol. 65: 863–866; 1999.