Increase of Rhinovirus Replication in Airway Epithelial Cells by Staphylococcal Enterotoxin A and B.
- Author:
Yong Ju JANG
1
;
Jong Hwan WANG
;
Hyun Ja KWON
;
Yoo Sam CHUNG
;
Bong Jae LEE
Author Information
1. Department of Otolaryngology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea. bjlee@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Rhinovirus;
Staphylococcal enterotoxin;
Staphylococcus aureus;
Chronic sinusitis
- MeSH:
Enterotoxins*;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells*;
Flow Cytometry;
Intercellular Adhesion Molecule-1;
Nasal Mucosa;
Rhinovirus*;
Staphylococcus aureus
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2006;49(11):1071-1076
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES : The toxins generated from Staphylococcus aureus, Staphylococcal enterotoxin A (SEA) and B (SEB), are reported to have an important role in the pathogenesis of chronic rhinosinusitis. As a basic step for elucidating the pathophysiologic responses of the nasal mucosa of chronic rhinosinusitis associated with rhinovirus infection, this study investigated the effect of SEA and SEB on rhinovirus infection in A549 cells. MATERIALS AND METHOD : The effect of SEA and SEB on the rhinovirus-induced changes in intercellular adhesion molecule-1 (ICAM-1) expression was assessed by flow cytometry. The effect of staphylococcal toxins on the rhinovirus-induced cytokine secretion was measured by ELISA. The effect of the replication of rhinovirus in the cells was examined by viral culture with subsequent determination of viral titer. RESULTS : ICAM-1 expression was increased in the rhinovirus infection group. Cytokine secretion was also increased in the rhinovirus infection group. But there was no additional increase due to staphylococcal toxins regarding the ICAM-1 expression and cytokine secretions. Staphylococcal toxins increased viral titer in proportion to toxin concentrations. CONCLUSION : SEA and SEB increased rhinoviral replication in airway epithelial cells. This result shows that airway epithelial cells with chronic rhinosinusitis are more favorable environments for rhinovirus infection.
