<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Papi, A.</style></author><author><style face="normal" font="default" size="100%">Papadopoulos, N. G.</style></author><author><style face="normal" font="default" size="100%">Stanciu, L. A.</style></author><author><style face="normal" font="default" size="100%">Degitz, K.</style></author><author><style face="normal" font="default" size="100%">Holgate, S. T.</style></author><author><style face="normal" font="default" size="100%">Johnston, S. L.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effect of desloratadine and loratadine on rhinovirus-induced intercellular adhesion molecule 1 upregulation and promoter activation in respiratory epithelial cells</style></title><secondary-title><style face="normal" font="default" size="100%">J Allergy Clin Immunol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Asthma Bronchi Epithelial Cells HeLa Cells Histamine H1 Antagonists Humans Intercellular Adhesion Molecule-1 Loratadine NF-kappa B Promoter Regions</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Respiratory Mucosa Rhinovirus Transcriptional Activation Up-Regulation</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11496238</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">2</style></number><volume><style face="normal" font="default" size="100%">108</style></volume><pages><style face="normal" font="default" size="100%">221-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Rhinoviruses have been recently associated with the majority of asthma exacerbations for which current therapy is inadequate. Intercellular adhesion molecule 1 (ICAM-1) has a central role in airway inflammation in asthma, and it is the receptor for 90% of rhinoviruses. Rhinovirus infection of airway epithelium induces ICAM-1. Desloratadine and loratadine are compounds belonging to the new class of H(1)-receptor blockers. Anti-inflammatory properties of antihistamines have been recently documented, although the underlying molecular mechanisms are not completely defined.|We have investigated the effects of desloratadine and loratadine on rhinovirus-induced ICAM-1 expression, mRNA upregulation, and promoter activation.|Cultured primary bronchial or transformed (A549) respiratory epithelial cells were pretreated with desloratadine and loratadine for 16 hours and infected with rhinovirus type 16 for 8 hours. ICAM-1 surface expression was evaluated with flow cytometry, and ICAM-1 mRNA was evaluated with specific RT-PCR. In A549 cells promoter activation was evaluated with a chloramphenicol acetyltransferase assay, and binding activity of nuclear factor kappa B in nuclear extracts was evaluated with an electrophoretic mobility shift assay.|Desloratadine and loratadine (0.1-10 micromol/L) inhibited rhinovirus-induced ICAM-1 upregulation in both primary bronchial or transformed (A549) respiratory epithelial cells. In A549 cells the 2 compounds showed a dose-dependent inhibition with similar efficacy (inhibitory concentration of 50%, 1 micromol/L). Desloratadine and loratadine also inhibited ICAM-1 mRNA induction caused by rhinovirus infection in a dose-dependent manner, and they completely inhibited rhinovirus-induced ICAM-1 promoter activation. Desloratadine also inhibited rhinovirus-induced nuclear factor kappa B activation. Desloratadine and loratadine had no direct effect on rhinovirus infectivity and replication in cultured epithelial cells.|These effects are unlikely to be mediated by H(1)-receptor antagonism and suggest a novel mechanism of action that may be important for the therapeutic control of virus-induced asthma exacerbations.</style></abstract><work-type><style face="normal" font="default" size="100%">Journal Article</style></work-type></record></records></xml>