Effect of loratadine on nitrogen dioxide-induced changes in electrical resistance and release of inflammatory mediators from cultured human bronchial epithelial cells.
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 NO2-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 NO2.


RESULTS
Exposure for 6 hours to NO2 significantly decreased the electrical resistance of HBEC cultures by 18.1% from baseline (P <.05). Incubation with 0.25 to 25 micromol/L loratadine did not alter the NO2-induced decrease in the electrical resistance of HBEC cultures. NO2 also significantly increased the release of IL-8 from a control value of 52.5 pg/microgram cellular protein to 81.9 pg/microgram cellular protein (P <.05), RANTES from a control value of 0.023 pg/microgram cellular protein to 0.062 pg/microgram cellular protein (P <.05), and sICAM-1 from a control value of 7.7 pg/microgram cellular protein to 16.3 pg/microgram cellular protein (P <.05). The NO2-induced release of all 3 mediators was significantly attenuated by incubation of HBECs with 25 micromol/L loratadine. Incubation with 2.5 micromol/L loratadine also significantly attenuated the NO2-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.
Bayram
H
H
Academic Department of Respiratory Medicine, St Bartholomew's and the Royal London School of Medicine and Dentistry, The London Chest Hospital, London, United Kingdom.
Devalia
J L
JL
Khair
O A
OA
Abdelaziz
M M
MM
Sapsford
R J
RJ
Czarlewski
W
W
Campbell
A M
AM
Bousquet
J
J
Davies
R J
RJ
D000328:Adult; D001980:Bronchi / Q000166:cytology*; D002478:Cells, Cultured; D018946:Chemokine CCL5 / Q000378:metabolism; D017097:Electric Impedance; D004847:Epithelial Cells / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D017336:Loratadine / Q000494:pharmacology*; D008875:Middle Aged; D009585:Nitrogen Dioxide / Q000494:pharmacology*; D012995:Solubility; D013997:Time Factors
D018946:Chemokine CCL5; D018836:Inflammation Mediators; D016209:Interleukin-8; D018799:Intercellular Adhesion Molecule-1; D017336:Loratadine; D009585:Nitrogen Dioxide