BACKGROUND AND OBJECTIVES: The presence of eosinophil-specific cytotoxic mediators in nasopharyngeal secretions of infants with more severe RSV infection in the respiratory tract suggests that eosinophils play a key role in the pathogenesis of RSV-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 effect of RSV infection on the expression 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 cells in flow cytometry and in the semi-quantitative RT-PCR. CD11b/CD18 on eosinophils was highly expressed by the RSV conditioned 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 suggested that pIgR expression in the epithelial cells may be a key factor for eosinophil degranulation via interaction with CD11b/CD18 in the RSV-infected epithelial cells.
Antibodies, Monoclonal ; Culture Media, Conditioned ; Eosinophils* ; Epithelial Cells* ; Flow Cytometry ; Humans ; Infant ; Inflammation ; Membranes ; Polymers* ; Receptors, Polymeric Immunoglobulin* ; Respiratory Syncytial Viruses* ; Respiratory System