Mediators of Inflammation

Mediators of Inflammation / 2001 / Article

Open Access

Volume 10 |Article ID 984605 |

Ilse Beckmann, Shlomo Ben-Efraim, Monica Vervoort, Henk C. S. Wallenburg, "Release of tumor necrosis factor-α and prostanoids in whole blood cultures after in vivo exposure to low-dose aspirin", Mediators of Inflammation, vol. 10, Article ID 984605, 8 pages, 2001.

Release of tumor necrosis factor-α and prostanoids in whole blood cultures after in vivo exposure to low-dose aspirin


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-α (TNF-α). 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-α, prostanoid E2 (PGE2) and prostanoid I2 (PGI2), and thromboxane A2 (TXA2). TNF-α and prostanoids were determined by enzyme-linked immunoassays.Results: In seven subjects, TNF-α release in blood cultures decreased 24 h 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 individua2l. The presence of DFU, a specific inhibitor of cyclooxygenase 2, did not affect the reduction of TNF-α release by aspirin, but abolished prostanoid production in all three individuals.Conclusion: The capacity of activated leukocytes to release TNF-α is reduced by ingestion of low-dose aspirin, independent of changes in prostanoid biosynthesis.

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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