Staphylococcus aureus Enterotoxin B Regulates Prostaglandin E2 Synthesis, Growth, and Migration in Nasal Tissue Fibroblasts

BackgroundSuperantigens and eicosanoids are important amplifiers and regulators of inflammation in airway diseases. We therefore studied the possible influence of Staphylococcus aureus enterotoxin B (SEB) on the cyclooxygenase (COX) pathway and basic functions of airway structural cells MethodsFibroblasts were isolated from nasal inferior turbinate tissue and cultured in the presence of different concentrations of SEB. Preincubation with interferon (IFN)–γ was performed to induce expression of major histocompatibility complex (MHC) class II receptors. Prostaglandin E2 (PGE2) production was assayed by enzyme-linked immunosorbent assay, and levels of COX-2 and prostanoid E receptors 1–4 (EP1–4) were assayed by real-time polymerase chain reaction. Migration and growth tests were performed, and SEB was localized within the cells by confocal microscopy ResultsStimulation with IFN-γ and SEB significantly down-regulated PGE2, COX-2, and EP2 expression but not EP1, EP3, or EP4 expression. The enterotoxin blocked cell growth but increased the fibroblast migration rate. SEB was localized within the cell in the presence and absence of MHC-II, suggesting that mechanisms other than conventional binding may allow the enterotoxin to enter the cell ConclusionsThese findings may have major implications for our understanding of the role played by bacterial superantigens in regulating the inflammatory and remodeling mechanisms of upper airway diseases and hence may help elucidate the pathophysiology of these diseases