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    Effect of desloratadine and loratadine on rhinovirus-induced intercellular adhesion molecule 1 upregulation and promoter activation in respiratory epithelial cells.

    Papi, A; Papadopoulos, N G; Stanciu, L A; Degitz, K; Holgate, S T; Johnston, S L

    The Journal of allergy and clinical immunology. 2001;108(2):221-8.

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    Abstract

    BACKGROUND: 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. OBJECTIVE: We have investigated the effects of desloratadine and loratadine on rhinovirus-induced ICAM-1 expression, mRNA upregulation, and promoter activation. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

    Bibliographic metadata

    Type of resource:
    Content type:
    Publication type:
    Published date:
    Abbreviated journal title:
    ISSN:
    Place of publication:
    United States
    Volume:
    108
    Issue:
    2
    Pagination:
    221-8
    Digital Object Identifier:
    10.1067/mai.2001.116861
    Pubmed Identifier:
    11496238
    Pii Identifier:
    S0091-6749(01)54313-4
    Access state:
    Active

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    Academic department(s):

    Record metadata

    Manchester eScholar ID:
    uk-ac-man-scw:240918
    Created by:
    Turner, Katie
    Created:
    26th November, 2014, 10:16:42
    Last modified by:
    Turner, Katie
    Last modified:
    26th November, 2014, 10:16:42

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