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Background and Objectives:The presence of eosinophil-specific cytotoxic mediators in nasopharyngeal secretions of infants induced airway inflammation and the associated epithelial damage. A recent report demonstrated that RSV-infected respiratory cells induce eosinophil degranulation by a CD11b/CD18-dependent, ICAM-1-independent mechanism. However, the molecule on the epithelial cell membrane involved in the receptor-mediated degranulation of eosinophils after RSV infection has not been clearly identified. Materials and Method:We investigated the efect of RSV infection on the expresion of pIgR on A549 cells and blocking of the RSV-infected cell induced eosinophil degranulation with monoclonal antibodies of the pIgR. Results:After 24h of RSV infection, A549 cells expressed pIgR remarkably whereas pIgR was hardly expressed by the uninfected cels in flow cytometry and in the semi-quantitative RT-PCR. CD11b/CD18 on eosinophils was highly expresed by the RSV con-ditioned media. Purified eosinophils cocultured with the RSV-infected A549 cells showed approximately eightfold increase in ECP in the isotype control, compared with the control and that was blocked by treatment of anti-pIgR monoclonal antibody. Conclusion:It is strongly sugested that pIgR expression in the epithelial cells may be a key factor for eosinophil degranula-(Korean J Otolaryngol 2003 ;46 :481-7)

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