Abstract
Background: Chronic rhinosinusitis (CRS) is an inflammatory disease. Excessive NLRP3 inflammasome activation and it’s downstream responses, plays a role in the pathogenesis of CRS. The context and purpose of the study: The aim of the study was to elucidate the effect of Staphylococcus aureus and budesonide on the mRNA expression and the biologic role (caspase-1 activation and IL-1β secretion) of NLRP3 inflammasome in primary nasal epithelial cells (NECs) in CRS patients and healthy controls.
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