Cellular Responses to @entity794 Alpha-Toxin in Chronic Rhinosinusitis with XXXX .

@entity1 @entity1712 @entity748 @entity794 @entity11765 @entity688 @entity1030 @entity91 @entity480
Background: In contrast to @entity794 -derived superantigenic exotoxins, the role of non-superantigenic exotoxins in the pathogenesis of eosinophilic @entity1030 remains obscure. We sought to characterize @entity794 alpha-toxin-induced cellular responses in chronic rhinosinusitis with @entity480 (CRSwNP). Methods: Dispersed nasal polyp cells and uncinate tissue cells were prepared from @entity1 with @entity91 with and without @entity480 , respectively. Cells were incubated with various concentrations of alpha-toxin or staphylococcal enterotoxin B and then the levels of IL-5, IL-13, IFN-y, IL-17A, and @entity688 in the cell supernatants were determined. The pathophysiological significance of alpha-toxin-induced cytokine production was also determined including radiological severity of rhinosinusitis, tissue and blood @entity1712 , serum total IgE level, and 1-s forced expiratory volume/forced vital capacity ratio (FEV1/FVC). Results: Nasal polyp cells produced substantial amounts of IL-5, IL-13, IFN-y, IL-17A, and @entity688 in response to alpha-toxin. Cytokine production was higher in nasal polyp cells than in uncinate tissue cells. The potency of alpha-toxin in stimulating IL-5, IL-13, and @entity688 production was comparable to that of @entity11765 . Alpha-toxin-induced IFN-y, IL-17A, and @entity688 production significantly and negatively correlated with the degree of eosinophil infiltration into @entity480 . Conversely, alpha-toxin-induced IFN-y and @entity688 production significantly and positively correlated with FEV1/FVC. @entity688 production was significantly lower in @entity748 @entity1 compared to non-asthmatics Conclusions: @entity794 -derived alpha-toxin can provoke cellular responses in @entity480 . These responses, especially failure to synthesize @entity688 , may play a role in the pathophysiology of CRSwNP.
