Original article Quantitative ¯ow cytometric analysis of the effects of cetirizine on the expression of ICAM-1/CD54 on primary cultured nasal cells An in vitro ¯ow cytometric model has been developed to evaluate the effects of antiallergic drugs such as cetirizine (CTZ) on the expression of surface molecules on primary cultured normal cells. Quantitative analysis demonstrated that HLA class I and ICAM-1/CD54 molecules are present on both epithelial and stromal cells, and that their expression is strongly enhanced by treatment with interferon- gamma (IFN-c). Nevertheless, the IFN-c-mediated upregulation of ICAM-1/ CD54 was inhibited by treatment with CTZ, demonstrating a direct effect on both cell types. This ®nding is particularly interesting because ICAM-1/CD54 is the main rhinovirus receptor, and rhinoviruses are the principal cause of asthma exacerbation in children. Thus, according to data derived from this in vitro model, CTZ should have an important role in the reduction of infectious exacerbation of asthma in atopic patients. M. Mincarini, F. Cagnoni, G. W. Canonica Servizio di Allergologia ed Immunologia Clinica, DIMI, Universita Á di Genoa, Genoa G. Cordone, A. Sismondini Dipartimento di Otorinolaringoiatria, Universita Á di Genova, Genoa C. Semino, G. Pietra, G. Melioli Servizio di Citometria, Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy Key words: cetirizine; CD54 (ICAM-1); epithelial cells; ®broblast; ¯ow cytometry. Giorgio Walter Canonica, MD Servizio di Allergologia ed Immunologia Clinica Dipartimento di Medicina Interna (DIMI) Largo R. Benzi, 10 16132 Genoa Italy Accepted for publication 28 October 1999 At present there is a general consensus that in¯amma- tion is crucial in the pathophysiology of respiratory allergic disease (1). In this context, adhesion molecules, a family of surface structures responsible for cell-to-cell interactions, have recently been described as playing a central role (2). For example, it is well known that ICAM-1/CD54 is deeply involved in virtually all immune reactions in both physiologic and pathologic conditions (3±6). In allergic patients, several studies have demonstrated the strict correlation between ICAM-1/CD54 expression on epithelial cells at the nasal and conjunctival levels and both the severity of clinical manifestations and the amount of allergic pressure (7, 8). In addition, in vitro studies have demonstrated that ICAM-1/CD54 is the main receptor for human rhinoviruses (9, 10). This characteristic is of great basic and clinical interest because it has been exhaustively shown that rhinoviruses represent the most frequent agent of the common cold (approximately 50% of cases), and in childhood, the exacerbation of asthma is usually associated with upper respiratory viral infections (11). Cetirizine (CTZ), the carboxylated metabolite of hydroxyzine, is a second-generation H 1 - antagonist with antiallergic properties, as demonstrated by its ef®cacy in reducing both the accumulation of eosinophils and the expression in vivo of ICAM-1/CD 54 at the nasal and conjunctival levels after allergenic challenge (12). In addition, we have already demon- strated in vivo, by immunocytochemical means, that CTZ is able to downregulate ICAM-1/CD54 on epithelial cells, but it is still unknown whether this is due to direct action on epithelial cells, or whether it occurs through different target cells (12, 13). Previous studies have demonstrated the possibility of modulating ICAM-1/CD54 on monoclonal cell lines by antiallergic drugs by semiquantitative immunochemis- try or immunoenzymatic methods (5). In this study, we established an in vitro model consisting of primary cultures of epithelial and stromal cells from surgical specimens of patients who underwent nasal surgery for polyposis and turbinate hypertrophy. The effects of CTZ on the surface expression modulation of ICAM-1/ CD54 and HLA I class antigens were assessed by quantitative ¯ow cytometric analysis both in basal conditions and during activation of the tested cells due to the addition of IFN-c to the medium culture. Allergy 2000: 55: 226±231 Printed in UK. All rights reserved Copyright # Munksgaard 2000 ALLERGY ISSN 0105-4538 226