METHODS: HNECs cultured at air-liquid interface were stimulated basally with 5ng/mL IL-13 in the presence or absence of omeprazole. Apical ASL pH was measured using a pH-sensitive SNARF-dextran dye. Nasal secretions were collected from control and CRS patients and pH was measured using a micro-pH meter. Inflammatory cytokine levels in nasal tissue from the same patients were assessed by Luminex assay.
RESULTS: The ASL pH from IL-13-stimulated HNECs (7.20±0.38) was significantly acidified compared to the ASL pH from unstimulated cells (7.39±0.32; P=0.03). Omeprazole prevented IL-13-induced acidification of ASL pH (7.39±0.35; P=0.004). Furthermore, the pH of nasal secretions was acidified in CRSwNP (6.16±0.54) compared to control (6.56±0.28; P=0.006) patients. Nasal secretion pH was significantly negatively correlated with type-2 cytokine levels, including IL-13, IL-4, and IL-5 (all p<0.05).
CONCLUSIONS: IL-13 acidified ASL pH in vitro and this was inhibited by omeprazole. Type-2-mediated inflammation in vivo was associated with acidified ASL pH in CRSwNP patients. Inhibition of IL-13-induced ASL pH acidification may provide therapeutic benefits to CRSwNP patients.