Key result
Low-dose aspirin significantly increased unstimulated ex vivo secretion of sIL-1RII compared to unmedicated controls (1115 vs 460 pg/mL, P=0.02).
Why the study?
Does low-dose aspirin increase soluble IL-1 receptor type II concentrations in healthy young men?
Observational
Does low-dose aspirin increase soluble IL-1 receptor type II concentrations in healthy young men?
Absolute Event Rate: 1115% vs 460%
p-value: p=0.02
Low-dose aspirin may exert anti-inflammatory effects by increasing the secretion of soluble IL-1 receptor type II, which prevents IL-1 from binding to target cells.
May support aspirin's anti-inflammatory effects via sIL-1RII; hypothesis-generating and requires in vivo confirmation before clinical consideration.
This study examined the influence of low-dose aspirin on interleukin (IL)-1alpha , 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-1beta 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 microg/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.
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Daun et al. (1999) conducted an observational in Healthy. Aspirin vs. Unmedicated controls was evaluated on Unstimulated ex vivo secretion of sIL-1RII (pg/mL) (p=0.02). Low-dose aspirin significantly increased unstimulated ex vivo secretion of sIL-1RII compared to unmedicated controls (1115 vs 460 pg/mL, P=0.02).
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