Role of P2X7R in eosinophilic and non-eosinophilic chronic rhinosinusitis with nasal polyps

Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammation-mediated disease of the nasal mucosa. P2X7R has been reported to be a potential biomarker for inflammation. The aim of the present study was to explore the role of P2X7R in CRSwNP, and the interaction between P2X7R and the NLRP3 inflammasome in the development of CRSwNP. Firstly, the expression profiles of P2X7R in nasal mucosa were investigated using western blotting (WB), polymerase chain reaction (PCR) and immunofluorescence (IF) staining. Next, the effect of inflammatory stimulation with lipopolysaccharides (LPS) combined with 2 '(3 ')-O-(4-benzoylbenzoyl) adenosine 5 '-triphosphate triethylammonium salt (BzATP) on primary human nasal epithelial cells (HNECs) was determined. Then, the therapeutic effect of the selective P2X7R antagonist, A740003, on P3X7R, NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome and IL-1 beta alterations in HNECs was explored using enzyme-linked immunosorbent assay, WB and PCR. It was found that P2X7R was overexpressed in CRSwNP, especially in eosinophilic CRSwNP, the expression of P2X7R, NLRP3 and IL-1 beta were upregulated in HNECs after induction by LPS combined with BzATP; but the expression of NLRP3 and IL-1 beta were downregulated after stimulation with A740003. The aforementioned results indicate that P2X7R-mediated NLRP3 inflammasome activation may have a role in the pathogenesis of CRSwNP.

Automated summary

The study investigated the role of P2X7R in chronic rhinosinusitis with nasal polyps (CRSwNP) and the interaction with the NLRP3 inflammasome. Results showed that P2X7R, NLRP3, and IL-1 beta were upregulated in primary human nasal epithelial cells (HNECs) after inflammatory stimulation, but downregulated after treatment with the P2X7R antagonist. These findings suggest that P2X7R-mediated NLRP3 inflammasome activation may play a role in the pathogenesis of CRSwNP.