Details

Autor(en) / Beteiligte

• Çelik, G.
• Bavbek, S.
• Misirligil, Z.
• Melli, M.

Titel

Release of cysteinyl leukotrienes with aspirin stimulation and the effect of prostaglandin E 2 on this release from peripheral blood leucocytes in aspirin‐induced asthmatic patients

Ist Teil von

• Clinical and experimental allergy, 2001-10, Vol.31 (10), p.1615-1622

Erscheinungsjahr

2001

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Background The decrease in prostaglandin E 2 (PGE 2 ) release due to aspirin (ASA)‐induced cyclooxygenase inhibition and the increment in cysteinyl leukotriene (Cys‐LT) release secondary to the removal of the inhibitory effect of PGE 2 on Cys‐LT release have been suggested in the pathogenesis of aspirin‐induced asthma (AIA). Objective In this study, we aimed to investigate the in vitro release of Cys‐LT and to determine the effect of PGE 2 on Cys‐LT release from peripheral blood leucocytes of patients with AIA after stimulation by ASA. Patients and methods Patients with AIA ( n  = 13), patients with ASA‐tolerant asthma (ATA) ( n  = 12) and healthy volunteers as controls ( n  = 13) were included to the study. ASA and PGE 2 at three different concentrations were applied to the peripheral blood leucocytes of the study group, and Cys‐LT levels following stimulants were assessed by enzyme immunoassay method. Results There was no difference in baseline Cys‐LT levels between groups (AIA 353.4 ± 55.5 pg/mL, ATA 354.7 ± 40.3 pg/mL, and control group 368.5 ± 30.2 pg/mL; P  > 0.05). Though not present in other groups, the Cys‐LT level of 453.6 ± 70.0 pg/mL following ASA stimulation was higher than baseline in patients with AIA ( P  = 0.04). When PGE 2 was added to the ASA‐stimulated samples of patients with AIA, Cys‐LT levels were measured as 298.7 ± 78.6 pg/mL, 279.8 ± 79.9 pg/mL, and 243.4 ± 51.3 pg/mL at PGE 2 10 −7   m , 10 −6   m and 10 −5   m concentrations, respectively. These levels were lower than the ASA‐stimulated Cys‐LT values ( P  = 0.03, P  = 0.01 and P  = 0.01, respectively). The inhibitory effect of different PGE 2 concentrations on Cys‐LT release was also present in patients with ATA and in controls. Conclusion The increase in Cys‐LT levels following ASA stimulation seems to be unique to AIA, which was not present in patients with ATA and in healthy controls. The inhibitory effect of PGE 2 on stimulated Cys‐LT levels is another important finding to elucidate the role of PGE 2 in the pathogenesis of AIA.