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Pharmacologic heterogeneity of human lung and colon cells: effect of terfenadine and cetirizine
Author(s) -
Fabre J. M.,
MartyAne C.,
Alauzen M.,
Souques F.,
Bousquet J.,
Campbell A. M.
Publication year - 1995
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.1398-9995.1995.tb01161.x
Subject(s) - terfenadine , cetirizine , leukotriene c4 , pharmacology , prostaglandin d2 , chemistry , immunoglobulin e , leukotriene , prostaglandin e2 , eicosanoid , prostaglandin , arachidonic acid , endocrinology , medicine , immunology , enzyme , asthma , biochemistry , antibody
H 1 ‐blockers may have antiallergic properties which cause the blocking of eicosanoid release, and the effect of these drugs may differ according to the phenotype of mast cells. This study examined the ability of terfenadine and cetirizine to inhibit the release of arachidonic acid‐derived mediators from human lung and colon cells. Dispersed cells were challenged with anti‐IgE in the presence or absence of 10 μM of terfenadine or cetirizine, and the release of prostaglandin (PG)D 2 and leukotriene (LT)C 4 /D 4 was assessed by enzyme immunoassay (EIA). Terfenadine caused significant inhibition of both PGD 2 and LTC 4 /D 4 (49 ±9 and 29 ± 19%, respectively) from human lung cells but had a less marked effect on PGD 2 release from human colon cells (21 ± 9% for PGD 2 and 18 ± 9% for LTC 4 /D 4 ). In contrast, although cetirizine caused significant inhibition of both mediators measured in lung cells (38 ± 16% for PGD 2 and 34 ± 19% for LTC 4 ), it did not cause any significant inhibition of either mediator from human colon cells. These findings suggest that H 1 antagonists may have additional properties, and the differential effects of cetirizine on lung and colon tissue may indicate differences in mast cell phenotype.