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Fluticasone Propionate Downregulates Nasal Fibroblast Functions Involved in Airway Inflammation and Remodeling

2002; Karger Publishers; Volume: 128; Issue: 1 Linguagem: Inglês

10.1159/000058003

1423-0097

Michela Silvestri, Federica Sabatini, Lucia Scarso, Annalisa Cordone, Gorana Dašić, Antônio Rossi,

Neuropeptides and Animal Physiology

<i>Background:</i> Besides being highly effective in the treatment of allergic and nonallergic rhinitis with eosinophilia, intranasal corticosteroids appear to be useful in reducing nasal polypoid lesions and the likelihood of polyp recurrence after surgery. We evaluated the ability of fluticasone propionate to downregulate fibroblast functions related to nasal inflammation and remodeling. <i>Methods:</i> Primary nasal polyp tissue-derived fibroblasts were stimulated with tumor necrosis factor (TNF)-α or interleukin (IL)-4 or basic fibroblast growth factor (bFGF) in the presence of fluticasone propionate (0.1–100 n<i>M</i>). Fibroblast proliferation, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expression and eotaxin release were then evaluated. <i>Results:</i> As compared with unstimulated cultures, a significant increase in fibroblast proliferation was observed when the cells were stimulated with bFGF (p < 0.05), but not with TNF-α or IL-4 (p > 0.05). TNF-α induced an upregulation of ICAM-1 expression (p < 0.05), which was not seen in fibroblasts cultured in the presence of IL-4 or bFGF. No changes in VCAM-1 expression were induced by TNF-α, IL-4 or bFGF, whereas both TNF-α and IL-4 increased eotaxin release (p < 0.05). Both bFGF-induced fibroblast proliferation and TNF-α-induced ICAM-1 expression were significantly reduced by fluticasone, starting at the dose of 1 and 10 n<i>M</i>, respectively (p < 0.05). Fluticasone at concentrations of 1–100 n<i>M</i> effectively inhibited eotaxin release by TNF-α- or IL-4-stimulated fibroblasts (p < 0.05). <i>Conclusions:</i> The pharmacologic activity of fluticasone in patients with chronic upper airway inflammatory disease may include inhibition of resident fibroblast functions involved in airway inflammation and remodeling.