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.
Academic Department of Respiratory Medicine, St Bartholomew's and the Royal London School of Medicine and Dentistry, The London Chest Hospital, London, United Kingdom.
H
H
Bayram
J L
JL
Devalia
O A
OA
Khair
M M
MM
Abdelaziz
R J
RJ
Sapsford
W
W
Czarlewski
A M
AM
Campbell
J
J
Bousquet
R J
RJ
Davies
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