BACKGROUND: Staphylococcal enterotoxin A (SEA) and staphylococcal enterotoxin B (SEB) have been reported to be important in the pathogenesis of chronic rhinosinusitis (CRS). To elucidate the pathophysiological responses in the nasal mucosae of CRS patients associated with rhinovirus (RV) infection, we investigated the effects of SEA and SEB on RV infection in A549 cells. METHODS: Changes in expression of intercellular adhesion molecule (ICAM) 1 were assessed by flow cytometry, and effects on cytokine secretion were measured by ELISA. The changes of ICAM-1, IL-1beta, IL-6, and IL-8 mRNA were assayed by real-time polymerase chain reaction. The effect of RV replication in the cells was assessed by viral culture, followed by determination of viral titer. RESULTS: RV infection increased ICAM-1 expression and cytokine secretion, but the SEs did not further increase the RV-induced expression of ICAM-1, IL-1beta, IL-6, and IL-8 mRNA and protein. The SEs, however, induced dose-dependent increases in viral titer. CONCLUSION: SEA and SEB enhanced rhinoviral replication in airway epithelial cells, indicating that airway epithelial cells with CRS are more favorable environments for RV infection.
BACKGROUND: Staphylococcal enterotoxin A (SEA) and staphylococcal enterotoxin B (SEB) have been reported to be important in the pathogenesis of chronic rhinosinusitis (CRS). To elucidate the pathophysiological responses in the nasal mucosae of CRSpatients associated with rhinovirus (RV) infection, we investigated the effects of SEA and SEB on RV infection in A549 cells. METHODS: Changes in expression of intercellular adhesion molecule (ICAM) 1 were assessed by flow cytometry, and effects on cytokine secretion were measured by ELISA. The changes of ICAM-1, IL-1beta, IL-6, and IL-8 mRNA were assayed by real-time polymerase chain reaction. The effect of RV replication in the cells was assessed by viral culture, followed by determination of viral titer. RESULTS: RV infection increased ICAM-1 expression and cytokine secretion, but the SEs did not further increase the RV-induced expression of ICAM-1, IL-1beta, IL-6, and IL-8 mRNA and protein. The SEs, however, induced dose-dependent increases in viral titer. CONCLUSION: SEA and SEB enhanced rhinoviral replication in airway epithelial cells, indicating that airway epithelial cells with CRS are more favorable environments for RV infection.
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