Eosinophil activation is induced by epithelial cells from respiratory mucosa. A comparative study between healthy and inflammatory mucosa

BACKGROUND: TO investigate the effect of epithelial cells from respiratory mucose on eosinophil activation, PATIENTS AND METHODS: Epithelial cell cultures were obtained from healthy nasal mucose and nasal polyps. Eosinophils were isolated from peripheral blood and incubated with epithelial cell conditioned media (HECM) in the presence or absence of dexamethasone (10 mu M). Eosinophil survival, expression of EG(2) and CD69, and production of eosinophil cationic protein (ECP) and leukotriene C-4 (LTC4) were evaluated. Cytokine levels in HECM were assessed by ELISA. RESULTS: HECM induced eosinophil survival (78.6 +/- 9.9% for nasal mucosa, and 92.6 +/- 15% for nasal polyps) compared to controls (1 +/- 0.8%; p < 0.05). Dexamethasone blocked HECM induced eosinophil survival, this effect being greater when eosinophils were primed with nasal mucosa HECM. HECM promoted EG, expression in eosinophils (47.9 +/- 9.1% for nasal mucose, and 58.5 +/- 11.8% for nasal polyp) compared to controls (8.1 +/- 3.7%; p < 0.01). HECM had no effect on both CD69 expression and LTC, release but decreased ECP secretion. Levels of interleukin (IL)-8 (35,700 +/- 7,300 pg/ml), IL-1 beta (11.3 +/- 1.8 pg/ml) and TNF-alpha (38.2 +/- 11 pg/ml) on nasal polyps HECM were significantly higher than on nasal mucosa HECM (17,600 +/- 2,700, 5.4 +/- 0.7 and 16.8 +/- 1.4 pg/ml, respectively; p < 0.05). CONCLUSIONS: Epithelial cells from respiratory mucose proved to have potential to increase eosinophil survival and activation. The lower inhibitory effect of dexamethasone on nasal polyps induced eosinophil survival and activation may be caused by a higher release of eosinophil activating factors from nasal polyp epithelial cells (inflammed tissue) compared to nasal mucosa.