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Inhibition of mediator and cytokine release from dispersed nasal polyp cells by terfenadine
Author(s) -
Crampette I.,
Mainprice B.,
Bloom M.,
Bousauet J.,
Campbell A. M.
Publication year - 1996
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.1996.tb04622.x
Subject(s) - terfenadine , histamine , cytokine , tumor necrosis factor alpha , pharmacology , granulocyte macrophage colony stimulating factor , chemistry , immunoglobulin e , mechanism of action , basophil , in vitro , histamine h1 receptor , immunology , receptor , medicine , biochemistry , antibody , antagonist
The mechanism of action of H 1 ‐lockers requires elucidation because they may possess properties unrelated to the blockage of histamine at its receptor level. A study was performed with enzymatically dispersed cells obtained from nasal polyps to examine the effect of terfenadine (0.1–10 μmol) on the release of leukotrienes (LT) (LTC 4 /D 4 and LTB 4 ) after stimulation by anti‐IgE, and on the spontaneous release of cytokines (granulocyte/macrophage‐colony stimulating factor [GM‐CSF] and tumor necrosis factor‐alpha [TNF‐α]) released from cells cultured for 6 h. Terfenadine inhibited significantly, and in a dose‐dependent manner, the release of LTC 4 /D 4 , LTB 4 , TNF‐α, and GM‐CSF. IC 50 values were determined for LTC 4 /D, (8 μmol), LTB 4 (9.9 μmol), TNF‐α (6.1 μmol), and GM‐CSF (4 μmol). Terfenadine was found to possess new antiallergic properties with a novel in vitro model which mimics more closely inflammatory cells of allergic rhinitis or asthma.