BACKGROUND: Patients with reflux-related respiratory symptoms are frequently treated with proton pump inhibitors (PPI). It is unclear whether aspiration of gastric juice (GJ) from patients "on" PPI can provoke a similar bronchial inflammatory reaction than that observed in patients "off" medication. The goal of this study was to evaluate the effect of GJ from patients with and without PPI treatment on production of IL-8 by human primary bronchial epithelial cells (PBEC). STUDY: PBEC were exposed during 24 hours to GJ (1/1000) from patients "on" (n=10) and "off" (n=13) PPI and to nonacidic gastric components (pepsin and bile acids). IL-8 concentration in supernatant was measured with enzyme-linked immunosorbent assay. Endotoxin level in GJ samples was analyzed with a LAL assay. RESULTS: Exposure of PBEC to GJ from patients "on" PPI provoked a higher production of IL-8 than GJ from patients "off" PPI [279 pg/mL (36 to 498) vs. 11 pg/mL (9 to 27)]. A correlation was found between pH of GJ and IL-8 production (r=0.659, P=0.0006). No correlation was found between IL-8 production and concentration of bile acids or pepsin. Filtration (0.20 [mu]m) of GJ from patients "on" PPI reduced IL-8 production. A positive correlation was found between IL-8 production and endotoxin levels of GJ samples (1/1000) (r=0.654, P=0.0007). CONCLUSIONS: Exposure of bronchial epithelial cells to GJ from patients "on" PPI is able to induce high IL-8 production. These results suggest that aspiration of GJ in patients treated with PPI might still be able to provoke a significant bronchial inflammatory reaction.
BACKGROUND: Patients with reflux-related respiratory symptoms are frequently treated with proton pump inhibitors (PPI). It is unclear whether aspiration of gastric juice (GJ) from patients "on" PPI can provoke a similar bronchial inflammatory reaction than that observed in patients "off" medication. The goal of this study was to evaluate the effect of GJ from patients with and without PPI treatment on production of IL-8 by human primary bronchial epithelial cells (PBEC). STUDY: PBEC were exposed during 24 hours to GJ (1/1000) from patients "on" (n=10) and "off" (n=13) PPI and to nonacidic gastric components (pepsin and bile acids). IL-8 concentration in supernatant was measured with enzyme-linked immunosorbent assay. Endotoxin level in GJ samples was analyzed with a LAL assay. RESULTS: Exposure of PBEC to GJ from patients "on" PPI provoked a higher production of IL-8 than GJ from patients "off" PPI [279 pg/mL (36 to 498) vs. 11 pg/mL (9 to 27)]. A correlation was found between pH of GJ and IL-8 production (r=0.659, P=0.0006). No correlation was found between IL-8 production and concentration of bile acids or pepsin. Filtration (0.20 [mu]m) of GJ from patients "on" PPI reduced IL-8 production. A positive correlation was found between IL-8 production and endotoxin levels of GJ samples (1/1000) (r=0.654, P=0.0007). CONCLUSIONS: Exposure of bronchial epithelial cells to GJ from patients "on" PPI is able to induce high IL-8 production. These results suggest that aspiration of GJ in patients treated with PPI might still be able to provoke a significant bronchial inflammatory reaction.
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