چکیده (انگلیسی):

Background: In contrast to Staphylococcus aureus-derived superantigenic exotoxins, the role of nonsuperantigenic
exotoxins in the pathogenesis of eosinophilic airway diseases remains obscure. We sought to
characterize S. aureus alpha-toxin-induced cellular responses in chronic rhinosinusitis with nasal polyps
(CRSwNP).
Methods: Dispersed nasal polyp cells and uncinate tissue cells were prepared from patients with CRS with
and without nasal polyps, respectively. Cells were incubated with various concentrations of alpha-toxin or
staphylococcal enterotoxin B and then the levels of IL-5, IL-13, IFN-γ, IL-17A, and IL-10 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 eosinophilia, serum total IgE level,
and 1-s forced expiratory volumeforced vital capacity ratio (FEV1FVC).
Results: Nasal polyp cells produced substantial amounts of IL-5, IL-13, IFN-γ, IL-17A, and IL-10 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 IL-10 production was comparable to that of enterotoxin. Alpha-toxininduced
IFN-γ, IL-17A, and IL-10 production significantly and negatively correlated with the degree of eosinophil
infiltration into nasal polyps. Conversely, alpha-toxin-induced IFN-γ and IL-10 production significantly and
positively correlated with FEV1FVC. IL-10 production was significantly lower in asthmatic patients compared to
non-asthmatics
Conclusions: S. aureus-derived alpha-toxin can provoke cellular responses in nasal polyps. These responses,
especially failure to synthesize IL-10, may play a role in the pathophysiology of CRSwNP.