Cilomilast counteracts the effects of cigarette smoke in innate immunity responses of airway epithelial cells (Abstract/Comunicazione in atti di convegno)

Type
Label
  • Cilomilast counteracts the effects of cigarette smoke in innate immunity responses of airway epithelial cells (Abstract/Comunicazione in atti di convegno) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • PACE E., FERRARO M., UASUF C.G., GIARRATANO A., LA GRUTTA S., LIOTTA G., JOHNSON M., GJOMARKAJ M (2010)
    Cilomilast counteracts the effects of cigarette smoke in innate immunity responses of airway epithelial cells
    in ERS annual congress, Barcelona, 18-22 September
    (literal)
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  • PACE E., FERRARO M., UASUF C.G., GIARRATANO A., LA GRUTTA S., LIOTTA G., JOHNSON M., GJOMARKAJ M (literal)
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  • 36 (literal)
Rivista
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  • 54 (literal)
Note
  • Abstract (literal)
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  • IBIM CNR Palermo Italy (literal)
Titolo
  • Cilomilast counteracts the effects of cigarette smoke in innate immunity responses of airway epithelial cells (literal)
Abstract
  • Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke extracts (CSE) increase the expression of TLR4 and alter its activation in bronchial epithelial cells. Cilomilast, a phosphodiesterase 4 inhibitor, inhibits cigarette smoke-induced neutrophilia. The main goal of this study was to explore whether cilomilast, in a human bronchial epithelial cell line (16-HBE), is able to counteract some of the effects of CSE. In particular, the expression of TLR4 (by flow-cytometry), the release of IP-10 and of IL-8 (by ELISA), the chemotactic activity toward lymphocytes and neutrophils (by microchemotaxis chamber) and the phosphorylation of ERK and of IkBa (by western blot analysis) in CSE and LPS-stimulated 16-HBE were assessed. In LPS-stimulated 16-HBE, CSE increased TLR4 expression, reduced both the IP-10 release and the chemotactic activity toward lymphocyte and increased both the IL-8 release and the chemotactic activity toward neutrophils. Cilomilast counteracted these effects due to CSE exposure reducing the expression of TLR4, increasing both the release of IP-10 and the chemotactic activity toward lymphocytes and toward neutrophils. No significant effect was observed on the release of IL-8. All these effects mediated by cilomilast are associated with a reduced ERK1/2 phosphorylation and with an increased IkBa phosphorylation. In conclusion, the results of the present study provide compelling evidences that cilomilast may be considered a possible valid therapeutic option in controlling inflammatory processes present in smokers (literal)
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