Effect of fluticasone propionate on interleukin-12 and interferon-gamma production in patients affected by allergic bronchial asthma

Fluticasone propionate is a very effective topical treatment for asthma. Interleukin-12, which is produced by monocyte-macrophage and B lymphocytic cell lines, plays an important role in the induction of Th1 cells; whereas interferon-gamma (IFN-gamma), mainly produced by Th1 cells, exhibits a crucial effect on macrophage and natural killer cell activation. Since previous studies have demonstrated a reduced production of IL-12 and IFN-gamma in patients with allergic asthma, we examined whether fluticasone propionate therapy could influence the release of these cytokines in asthma. We selected two groups of subjects (15 per group): nonatopic healthy donors (group A) and asthmatic patients (group B). Cytokine release was assessed in sera as well as in supernatants of whole blood cultures after IFN-gamma priming and lipopolysaccharide stimulation. Venous blood and spirometric tests from patients in group B were obtained before and after treatment. Fluticasone propionate therapy significantly increased interleukin-12 levels in both supernatants of blood cultures (1,152.12 +/- 225.57 vs. 540.87 +/- 130.07 pg/ml; p0.05) or in sera (72.24 +/- 15.76 vs. 10.83 +/- 2.70 pg/ml; p0.05). Patients treated with fluticasone propionate also displayed increased levels of IFN-gamma in either blood culture supernatants (59.12 +/- 16.88 vs. 18.87 +/- 7.53 IU/ml; p0.05) or in sera (5.60 +/- 2.87 vs.1 IU/ml; p0.05). In addition, we observed a significant increase in FEV1 values in asthmatic patients after fluticasone propionate therapy (51.86 +/- 5.31 vs. 71.46 +/- 10.37% predicted). We propose that fluticasone propionate may exert at least in part of its antiinflammatory activity through the modulation of the cytokine output.