Key result
A single 80 mg dose of aspirin reduced the capacity of activated leukocytes to release TNF-alpha in 7 of 8 healthy subjects, independent of changes in prostanoid biosynthesis.
Why the study?
Does a single oral dose of 80 mg aspirin reduce the release of TNF-alpha and prostanoids in whole blood cultures from healthy subjects?
Does a single oral dose of 80 mg aspirin reduce the release of TNF-alpha and prostanoids in whole blood cultures from healthy subjects?
Low-dose aspirin reduces the capacity of activated leukocytes to release TNF-alpha independently of cyclooxygenase inhibition, suggesting an additional anti-inflammatory mechanism.
Suggests COX-independent anti-inflammatory action of low-dose aspirin; hypothesis-generating and requires validation in patients.
BACKGROUND: The preventive effect of low-dose aspirin in cardiovascular disease is generally attributed to its antiplatelet action caused by differential inhibition of platelet cyclooxygenase-1. However, there is evidence that aspirin also affects release of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha). It is not known whether this is caused by direct action on the cytokine pathway or indirectly through cyclooxygenase inhibition and altered prostanoid synthesis, or both. METHODS: We assessed the capacity of lipopolysaccharide-activated leukocytes in whole blood cultures of eight healthy subjects following a single oral dose of 80 mg aspirin to release TNF-alpha, prostanoid E2 (PGE2) and prostanoid I2 (PGI2), and thromboxane A2 (TXA2). TNF-alpha and prostanoids were determined by enzyme-linked immunoassays. RESULTS: In seven subjects, TNF-alpha release in blood cultures decreased 24h after intake of aspirin. The effect of aspirin on prostanoid release was assessed in three individuals: PGE2 increased in all subjects, PGI2 increased in two and remained unchanged in one, and TXA2 was reduced in two and unchanged in one individual The presence of DFU, a specific inhibitor of cyclooxygenase 2, did not affect the reduction of TNF-alpha release by aspirin, but abolished prostanoid production in all three individuals. CONCLUSION: The capacity of activated leukocytes to release TNF-alpha is reduced by ingestion of low-dose aspirin, independent of changes in prostanoid biosynthesis.
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Beckmann et al. (2001) studied Healthy (n=8). Aspirin was evaluated on Release of TNF-alpha in whole blood cultures. A single 80 mg dose of aspirin reduced the capacity of activated leukocytes to release TNF-alpha in 7 of 8 healthy subjects, independent of changes in prostanoid biosynthesis.
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