Cytokine-activated bronchial epithelial cell pro-inflammatory functions are effectively downregulated in vitro by ciclesonide

M. Silvestri, L. Serpero, L. Petecchia, F. Sabatini, F. Cerasoli, G. A. Rossi

Research output: Contribution to journalArticlepeer-review

Abstract

Ciclesonide, a new inhaled corticosteroid, is administered as a parent compound and converted in the airway mucosa into the active metabolite, desisobutyryl-(des-)ciclesonide. A study was designed to evaluate the ability of ciclesonide to modulate pro-inflammatory functions of human bronchial epithelial cell (HBEC) primary cultures being converted into des-ciclesonide. HBECs were stimulated with interleukin (IL)-4 and tumour necrosis factor (TNF)-α (20 ng/mL) in the presence of ciclesonide and intercellular adhesion molecule (ICAM)-1 expression, granulocyte-macrophage colony stimulating factor (GM-CSF) and IL-8 release evaluated respectively by FACS and ELISA. Ciclesonide (3 μM) significantly inhibited ICAM-1 expression by stimulated HBECs, already after 3 h and still after 48 h culture (p

Original languageEnglish
Pages (from-to)210-217
Number of pages8
JournalPulmonary Pharmacology and Therapeutics
Volume19
Issue number3
DOIs
Publication statusPublished - Jun 2006

Keywords

  • Adhesion molecule expression
  • Airway epithelial cells
  • Asthma
  • Chemokines
  • Ciclesonide
  • Cytokines

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Pharmacology

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