title: Inhibition of nasal polyp mast cell and eosinophil activation by desloratadine.
abstract: Nasal polyp tissue which contains mast cells and eosinophils is similar to the inflamed airway mucosa in cellular composition and mediator content. This investigation assessed the effect of desloratadine (DL), on activation of cells in nasal polyp tissue. Polyps were obtained from 22 patients with chronic rhinosinusitis [nine aspirin acetylosalitic acid (ASA)-sensitive and 13 ASA-tolerant]. Polyp tissue was dispersed by digestion, and preincubated with DL and incubated with anti-immunoglobulin E (IgE) or calcium ionophore. LTC4, eosinophil cationic protein (ECP) and tryptase concentrations in supernatants were measured by immunoassays. Desloratadine (1, 10 and 50 microM) inhibited calcium ionophore-induced LTC4 release by a mean of 29%, 50% and 63% respectively, and anti-IgE-induced LTC4 release by a mean of 27%, 35% and 39% respectively. Calcium ionophore-induced tryptase release was inhibited 60% and 69% by 10 and 50 microM of DL, respectively, and anti-IgE-induced tryptase release was inhibited 33%, 47% and 66% for 1, 10 and 50 microM of DL. Desloratadine 10 microM and 50 microM inhibited ECP release by and 45% and 48% respectively. Polyp tissue from ASA-sensitive patients when compared with ASA-tolerant patients released at baseline significantly more ECP (medians 120.0 microg/ml, range: 69.0-182.0 vs 63.4 microg/ml, range: 3.7-172.0; P <0.05), but similar amounts of tryptase and LTC4. This study demonstrated that DL inhibits activation of both eosinophils and mast cells derived from a site of airway mucosal inflammation.
authors.affiliation: Department of Clinical Immunology and Allergy, Faculty of Medicine, Medical University, Lodz, Poland.
authors.forename: M L
authors.initials: ML
authors.lastname: Kowalski
authors.forename: A
authors.initials: A
authors.lastname: Lewandowska
authors.forename: J
authors.initials: J
authors.lastname: Wozniak
authors.forename: J
authors.initials: J
authors.lastname: Makowska
authors.forename: A
authors.initials: A
authors.lastname: Jankowski
authors.forename: L
authors.initials: L
authors.lastname: DuBuske
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D001241:Aspirin / Q000009:adverse effects; D004342:Drug Hypersensitivity / Q000150:complications; D047150:Eosinophil Cationic Protein / Q000378:metabolism; D004804:Eosinophils / Q000378:metabolism*; D005260:Female; D039563:Histamine H1 Antagonists, Non-Sedating / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D017997:Leukotriene C4 / Q000378:metabolism; D017336:Loratadine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D008297:Male; D008407:Mast Cells / Q000378:metabolism*; D008875:Middle Aged; D009298:Nasal Polyps / Q000150:complications / Q000378:metabolism*; D012697:Serine Endopeptidases / Q000378:metabolism; D053802:Tryptases
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D039563:Histamine H1 Antagonists, Non-Sedating; D018836:Inflammation Mediators; D017997:Leukotriene C4; D017336:Loratadine; D047150:Eosinophil Cationic Protein; D012697:Serine Endopeptidases; D053802:Tryptases; C121345:desloratadine; D001241:Aspirin