Abstract
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.)
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