The Effect of Polymeric Immunoglobulin Receptor on Eosinophil Degranulation in Respiratory Syncytial Virus Infection of Respiratory Epithelial Cells.
- Author:
Sung Wan KIM
1
;
Joong Saeng CHO
;
Jae Myung KIM
;
Jun Yeon HWANG
;
Roberto GAROFALO
Author Information
1. Department of Otolaryngology, College of Medicine, Kyung Hee University, Seoul, Korea. khuent@khmc.or.kr
- Publication Type:Original Article
- Keywords:
Respiratory syncytial viruses;
Polymeric immunoglobulin receptors;
Eosinophils
- MeSH:
Antibodies, Monoclonal;
Culture Media, Conditioned;
Eosinophils*;
Epithelial Cells*;
Flow Cytometry;
Humans;
Infant;
Inflammation;
Membranes;
Polymers*;
Receptors, Polymeric Immunoglobulin*;
Respiratory Syncytial Viruses*;
Respiratory System
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2003;46(6):481-487
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
