In vitro activity: Fluticasone propionate (1 pM) inhibits the constitutive and TGF-beta-induced expression of alpha-SMA in human lung myofibroblasts. Fluticasone propionate blocks the TNF-alpha-induced nuclear translocation of the pro-inflammatory transcription factor NF-kappaB in human lung myofibroblasts. Fluticasone propionate inhibits in lung myofibroblasts, at a very early stage of differentiation, the activation of Janus kinase/STAT pathways induced by IL-13 (tyrosine kinase 2, STAT1, STAT3, STAT6, mitogen-activated protein kinase). Fluticasone propionate still displays a potential anti-inflammatory activity even if it only inhibits tyrosine kinase 2 phosphorylation in mildly or fully differentiated myofibroblastic cultures. Fluticasone propionate inhibits constitutive and TGF-beta-induced expression of alpha-smooth muscle actin, the main marker of myofibroblastic differentiation, both in very early and in mild differentiated myofibroblasts. Fluticasone propionate displays an additional powerful anti-inflammatory effect, decreasing nuclear translocation of NF-kappaB independent of the degree of myofibroblastic differentiation. Fluticasone propionate inhibits allergen-induced T-cell proliferation, expression of IL-3, IL-5 and GM-CSF mRNA, and secretion of the corresponding proteins in a concentration-dependent fashion. Fluticasone propionate has the potential markedly to inhibit allergen-induced T-cell production of asthma-relevant cytokines.