Pathogenesis of Nasal polyp has been primarily investigated on the basis of sinonasal mucosal immunity. Several inflammatory responses have been reported in nasal polyp pathogenesis to date. In this study the researchers have summarised new research on pathways for developing chronic nasal polyp rhinosinusitis (CRSwNP), which focuses on Th2 inflammation. The th2 inflammation may be driven by Staphylococcus aureus by the production of enterotoxins and a serine protease-like protein. Furthermore, S. aureus affected the activity of the mucosal obstruction directly and increased synthesis of Th2 cytokines by the rapid activation of endogenous epithelial cytokines. The synthesis of innate lymphoid epithelial-derived cytokines, including TSLP, IL-25, and IL-33, promotes th2 reactions. Mast cell produces IL-5, IL-13 and periostin and has a function to play in the pathogenesis of nasal polyps by orchestrating infiltration of eosinophils. The formation of extracellular eosinophil traps and Charcot-Leyden crystals is closely linked with the seriousness of disease and development of viscous mucus plugs.
The role of S. aureus in innate and adaptive immunity is increasingly evident and contributes to the inflammation of Th2 in CRSwNP. Innate immunity, like epithelial cytokines, is critical in the production of CRSwNP, inducing different pathways, and must be further examined as Th2-controlled biomarkers. Neutrophilic inflammation has recently begun to be investigated but still remains uncertain.
