Drugs online research references
Allergy. 1994 Apr;49(4):246-53.
In vitro effects of H1-antihistamines on histamine and PGD2 release from mast cells of human lung, tonsil, and skin.
Okayama Y, Benyon RC, Lowman MA, Church MK.
Immunopharmacology Group, Southampton General Hospital, UK.
Mast cells from different anatomic sites differ in cytochemistry and response to various secretory stimuli. We have investigated whether responsiveness to the second-generation H1-receptor antagonists, which are important first-line drugs for the relief of symptoms in patients with chronic urticaria and allergic rhinoconjunctivitis, also differs according to the site of origin of mast cells. The effects of terfenadine, ketotifen, and cetirizine were therefore examined in relation to the IgE-dependent release of histamine and prostaglandin D2 (PGD2) from dispersed human lung, tonsil, and skin mast cells. Terfenadine had a biphasic effect on lung and skin mast cells: at low concentrations, a concentration-dependent inhibition of histamine release from lung and skin mast cells was observed, whereas at higher concentrations the drug stimulated mediator release. Even at a high concentration, terfenadine inhibited mediator release from tonsil mast cells. Ketotifen had low potency as an inhibitor of mediator release from lung and tonsil mast cells. In skin mast cells, no inhibition of mediator release was observed below 1.0 microM, and above that concentration it induced mediator release. Cetirizine, a much less lipophilic drug than the others tested, did not induce mediator release from mast cells even at concentrations up to 100 microM. This drug showed concentration-dependent inhibition of IgE-dependent mediator release from lung and tonsil mast cells only. Our results show that human mast cells are heterogeneous with respect to modulation of mediator release by these H1-antihistamines. In particular, differences were observed between skin mast cells and those dispersed from lung and tonsils.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7518654&dopt=Abstract
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Allergy. 1995 Apr;50(4):362-5.
Pharmacologic heterogeneity of human lung and colon cells: effect of terfenadine and cetirizine.
Fabre JM, Marty-Ane C, Alauzen M, Souques F, Bousquet J, Campbell AM.
Clinique des Maladies Respiratoires and CJF-INSERM 92-10, Centre Hospitalier Universitaire, Montpellier, France.
H1-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 microM of terfenadine or cetirizine, and the release of prostaglandin (PG)D2 and leukotriene (LT)C4/D4 was assessed by enzyme immunoassay (EIA). Terfenadine caused significant inhibition of both PGD2 and LTC4/D4 (49 +/- 9 and 29 +/- 19%, respectively) from human lung cells but had a less marked effect on PGD2 release from human colon cells (21 +/- 9% for PGD2 and 18 +/- 9% for LTC4/D4). In contrast, although cetirizine caused significant inhibition of both mediators measured in lung cells (38 +/- 16% for PGD2 and 34 +/- 19% for LTC4), it did not cause any significant inhibition of either mediator from human colon cells. These findings suggest that H1-antagonists may have additional properties, and the differential effects of cetirizine on lung and colon tissue may indicate differences in mast cell phenotype.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7573821&dopt=Abstract
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Clin Exp Allergy. 1999 Dec;29(12):1681-91.
Cetirizine counter-regulates interleukin-8 release from human epithelial cells (A549)
Arnold R, Rihoux J, Konig W.
Institute of Medical Microbiology and Immunology, AG Infektabwehr, Ruhr-University, Bochum, Germany; Institute of Medical Immunology, Charite-Campus Mitte, Humboldt University, Berlin, Germany.
BACKGROUND: Cetirizine, a H1-receptor antagonist, exerts besides its well-known anti-allergic potential an array of anti-inflammatory activities. In particular epithelial cells activated in the presence of cetirizine showed a reduced ICAM-1 cell surface expression and a diminished release of sICAM-1. OBJECTIVE: We wondered whether cetirizine might influence the release of interleukin-8 (IL-8) from human epithelial cells activated with agonists distinct from histamine. METHODS: We used the human lung epithelial cell line A549 for our in vitro studies. IL-8 release was determined by IL-8 enzyme immunoassay, the intracellular staining for IL-8 and NF-kB was analysed by FACS analysis and IL-8 mRNA steady state level was studied by Northern blot analysis. Confluent epithelial cell monolayer were pre-incubated with cetirizine (0.01 -1.0 micromol/L) for 30 min and afterwards activated with pro-inflammatory cytokines (TNF-alpha IL-1beta, IL-6, IFN-gamma) or different agonists (PMA, NaF, respiratory syncytial virus [RSV]) for 24 h. RESULTS: Epithelial cells stimulated with TNF-alpha IL-1beta, PMA and RSV, respectively, showed a significantly increased release of IL-8. Pre-incubation with cetirizine diminished the IL-8 release from cells activated with TNF-alpha or PMA in a significant manner. The reduced IL-8 release coincided with a diminished percentage of cells expressing IL-8. Northern blot analysis revealed a reduced steady state level of IL-8 mRNA in cells pretreated with cetirizine and stimulated with TNF-alpha. Furthermore, a decreased amount of accessible DNA-binding sites of the nuclear factor kappa B (NF-kB) was determined by FACS analysis. CONCLUSIONS: These results suggest that cetirizine reduced the release of IL-8 from A549 cells stimulated with PMA and TNF-alpha, respectively, by lowering IL-8 gene expression. Therefore, cetirizine might exert anti-inflammatory effects beyond its H1-receptor antagonistic activity in the course of inflammatory respiratory tract disorders such as bronchial asthma and allergic rhinitis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10594545&dopt=Abstract
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