Fluticasone propionate downregulates nasal fibroblast functions involved in airway inflammation and remodeling

M. Silvestri, F. Sabatini, L. Scarso, A. Cordone, G. Dasic, Giovanni A. Rossi

Research output: Contribution to journalArticle

Abstract

Background: 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. Methods: 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 nM). Fibroblast proliferation, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expression and eotaxin release were then evaluated. Results: 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 nM, respectively (p <0.05). Fluticasone at concentrations of 1-100 nM effectively inhibited eotaxin release by TNF-α- or IL-4-stimulated fibroblasts (p <0.05). Conclusions: 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.

Original languageEnglish
Pages (from-to)51-58
Number of pages8
JournalInternational Archives of Allergy and Immunology
Volume128
Issue number1
DOIs
Publication statusPublished - 2002

Fingerprint

Airway Remodeling
Nose
Down-Regulation
Fibroblasts
Inflammation
Fibroblast Growth Factor 2
Interleukin-4
Tumor Necrosis Factor-alpha
Intercellular Adhesion Molecule-1
Vascular Cell Adhesion Molecule-1
Nasal Polyps
Fluticasone
Eosinophilia
Polyps
Adrenal Cortex Hormones
Up-Regulation
Recurrence

Keywords

  • Cell adhesion molecules
  • Cytokines
  • Inflammation
  • Nasal polyps

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Fluticasone propionate downregulates nasal fibroblast functions involved in airway inflammation and remodeling. / Silvestri, M.; Sabatini, F.; Scarso, L.; Cordone, A.; Dasic, G.; Rossi, Giovanni A.

In: International Archives of Allergy and Immunology, Vol. 128, No. 1, 2002, p. 51-58.

Research output: Contribution to journalArticle

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abstract = "Background: 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. Methods: 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 nM). Fibroblast proliferation, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expression and eotaxin release were then evaluated. Results: 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 nM, respectively (p <0.05). Fluticasone at concentrations of 1-100 nM effectively inhibited eotaxin release by TNF-α- or IL-4-stimulated fibroblasts (p <0.05). Conclusions: 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.",
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AU - Silvestri, M.

AU - Sabatini, F.

AU - Scarso, L.

AU - Cordone, A.

AU - Dasic, G.

AU - Rossi, Giovanni A.

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