Effect of loratadine on nitrogen dioxide–induced changes in electrical resistance and release of inflammatory mediators from cultured human bronchial epithelial cells

• Published in: Journal of allergy and clinical immunology Vol. 104; no. 1; pp. 93 - 99
• Main Authors: Bayram, Hasan, Devalia, Jagdish L., Khair, Omer A., Abdelaziz, Muntasir M., Sapsford, Raymond J., Czarlewski, Wienia, Campbell, Alison M., Bousquet, Jean, Davies, Robert J.
• Format: Journal Article
• Language: English
• Published: New York, NY Mosby, Inc 01.07.1999; Elsevier
• Subjects: Adult; Biological and medical sciences; Bronchi - cytology; bronchial epithelial cells; Cells, Cultured; Chemokine CCL5 - metabolism; Electric Impedance; Epithelial Cells - metabolism; Humans; Inflammation Mediators - metabolism; inflammatory mediators; Intercellular Adhesion Molecule-1 - metabolism; Interleukin-8 - metabolism; Loratadine; Loratadine - pharmacology; Medical sciences; Middle Aged; Nitrogen Dioxide - pharmacology; nitrogen dioxide electrical resistance; Pharmacology. Drug treatments; Respiratory system; Solubility; Time Factors; inflammatory mediators; sICAM-1; ECP; bronchial epithelial cells; HBEC; LTC 4; ICAM-1; nitrogen dioxide electrical resistance; NEC; Loratadine; SF-1 medium; Human; Intercellular adhesion molecule 1; RANTES; Cytokine; Cell adhesion molecule; Bronchus; Chemical mediator; Inflammation; Antihistaminic; In vitro; Biological activity; Epithelial cell; Antagonist; Nitrogen dioxide; Mechanism of action; H1 Histamine receptor; Interleukin 8
• ISSN: 0091-6749; 1097-6825
• DOI: 10.1016/S0091-6749(99)70119-3

Background: Recent studies have demonstrated that some antihistamines can attenuate histamine-induced release of inflammatory mediators from bronchial epithelial cells. Objective: The purpose of study was to test the hypothesis that loratadine may influence pollution-induced inflammation of the airways by modulating epithelial membrane integrity and the synthesis and/or release of inflammatory mediators from airway epithelial cells. Methods: We have cultured human bronchial epithelial cell (HBEC) cultures from surgical explants and investigated the effect of loratadine on NO 2 –induced changes in both electrical resistance of HBEC cultures and release of IL-8, RANTES, and soluble intercellular adhesion molecule-1 (sICAM-1) from these cells after exposure for 6 hours to either air or 400 ppb NO 2. Results: Exposure for 6 hours to NO 2 significantly decreased the electrical resistance of HBEC cultures by 18.1% from baseline ( P < .05). Incubation with 0.25 to 25 μmol/L loratadine did not alter the NO 2 –induced decrease in the electrical resistance of HBEC cultures. NO 2 also significantly increased the release of IL-8 from a control value of 52.5 pg/μg cellular protein to 81.9 pg/μg cellular protein ( P < .05), RANTES from a control value of 0.023 pg/μg cellular protein to 0.062 pg/μg cellular protein ( P < .05), and sICAM-1 from a control value of 7.7 pg/μg cellular protein to 16.3 pg/μg cellular protein ( P < .05). The NO 2 –induced release of all 3 mediators was significantly attenuated by incubation of HBECs with 25 μmol/L loratadine. Incubation with 2.5 μmol/L loratadine also significantly attenuated the NO 2 –induced release of RANTES and sICAM-1, but not IL-8. Conclusions: These results suggest that loratadine has the potential to reduce airway inflammation by modulating the release of inflammatory cytokines from airway epithelial cells. (J Allergy Clin Immunol 1999;104:93-9.)