BACKGROUND: Superantigens 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. METHODS: Fibroblasts were isolated from nasal inferior turbinate tissue and cultured in the presence of different concentrations of SEB. Preincubation with interferon (IFN)-gamma was performed to induce expression of major histocompatibility complex (MHC) class II receptors. Prostaglandin E2 (PGE(2)) production was assayed by enzyme-linked immunosorbent assay, and levels of COX-2 and prostanoid E receptors 1-4 (EP(1-4)) were assayed by real-time polymerase chain reaction. Migration and growth tests were performed, and SEB was localized within the cells by confocal microscopy. RESULTS: Stimulation with IFN-gamma and SEB significantly down-regulated PGE(2), COX-2, and EP(2) expression but not EP(1), EP(3), or EP(4) 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. CONCLUSIONS: These 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.
BACKGROUND: Superantigens 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. METHODS: Fibroblasts were isolated from nasal inferior turbinate tissue and cultured in the presence of different concentrations of SEB. Preincubation with interferon (IFN)-gamma was performed to induce expression of major histocompatibility complex (MHC) class II receptors. Prostaglandin E2 (PGE(2)) production was assayed by enzyme-linked immunosorbent assay, and levels of COX-2 and prostanoid E receptors 1-4 (EP(1-4)) were assayed by real-time polymerase chain reaction. Migration and growth tests were performed, and SEB was localized within the cells by confocal microscopy. RESULTS: Stimulation with IFN-gamma and SEB significantly down-regulated PGE(2), COX-2, and EP(2) expression but not EP(1), EP(3), or EP(4) 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. CONCLUSIONS: These 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.
Authors: Thad W Vickery; Michael Armstrong; Jennifer M Kofonow; Charles E Robertson; Miranda E Kroehl; Nichole A Reisdorph; Vijay R Ramakrishnan; Daniel N Frank Journal: Prostaglandins Leukot Essent Fatty Acids Date: 2020-11-26 Impact factor: 4.006
Authors: Laura Miek; Paul M Jordan; Kerstin Günther; Simona Pace; Timo Beyer; David Kowalak; Verena Hoerr; Bettina Löffler; Lorena Tuchscherr; Charles N Serhan; Jana Gerstmeier; Oliver Werz Journal: Immunology Date: 2022-03-09 Impact factor: 7.215