Fig. 1From: The role of Staphylococcus aureus enterotoxin B in chronic rhinosinusitis with nasal polyposisPossible mechanisms of SEB in inducing CRS and nasal polyposis. A SEB activates Toll Like Receptor 2 (TLR2) and triggers the production of pro-inflammatory cytokines; besides, it induces reactive oxygen species and endoplasmic reticulum stress-induced inflammation that may cause epithelial cell integrity disruption and enhance permeability. B Nasal fibroblast, especially nasal polyp fibroblast, and epithelial cells produce high levels of TSLP and result in Th2 differentiation and proliferation after exposure to SEB. C T regs 1 cell may reduce Th1 cells activity and increase the development of Th2 cells. D SEB-induced Typical type 2/Th2 pathway. E Th2-associated cytokines lead to the IgE production from plasma cells, eosinophils degranulation, the release of cationic proteins, and localized eosinophilic inflammation. F SEB could be involved in the further production of RORC+ Tregs, resulting in an increased production of inflammatory cytokines, which may contribute to the pathogenesis of eosinophilic nasal polyposisBack to article page