Upregulated TRPC5 plays an important role in development of nasal polyps by activating eosinophilic inflammation and NF-κB signaling pathways.

The pathophysiology of nasal polyps (NP) remains unclear, however, several ion channels may participate. Whether transient receptor potential canonical (TRPC) channel play a role in NP remains unknown. We investigated expression of TRPC, eosinophil infiltration, IL-6, and NF-κB in 58 patients with NP and 35 control subjects using hematoxylin-eosin (HE) staining, immunohistochemistry, real-time fluorescence quantitative reverse transcription PCR (real-time RT-PCR), Western blotting, and calcium imaging. Compared with normal nasal mucosa, TRPC5 mRNA and protein expression increased in NP. Eosinophil counts, IL-6 expression, and phosphorylation levels of NF-κB were higher in NP than in normal mucosa. TRPC5 expression was positively correlated with eosinophils, IL-6, and phosphorylation levels of NF-κB. Blocking of TRPC5 channel decreased store-operated calcium influx, IL-6 expression, and phosphorylation levels of NF-κB in blood eosinophils from patients with NP. In conclusion, TRPC5 was upregulated in NP and played an important role in development of NP by activating eosinophilic inflammation and NF-κB signal pathways.