Fluticasone induces apoptosis in peripheral T-lymphocytes: a comparison between asthmatic and normal subjects (Articolo in rivista)

Type
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  • Fluticasone induces apoptosis in peripheral T-lymphocytes: a comparison between asthmatic and normal subjects (Articolo in rivista) (literal)
Anno
  • 2002-01-01T00:00:00+01:00 (literal)
Alternative label
  • Melis M., Siena L., Pace E., Gjomarkaj M., Profita M., Pirazzoli A., Todaro M., Stassi G., Bonsignore G., Vignola Am. (2002)
    Fluticasone induces apoptosis in peripheral T-lymphocytes: a comparison between asthmatic and normal subjects
    in The European respiratory journal
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Melis M., Siena L., Pace E., Gjomarkaj M., Profita M., Pirazzoli A., Todaro M., Stassi G., Bonsignore G., Vignola Am. (literal)
Pagina inizio
  • 257 (literal)
Pagina fine
  • 266 (literal)
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  • 19 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
  • Impact Factor: 2.989 (literal)
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  • Studio sui meccanismi anti-infiammatori del fluticasone, uno steroide di ultima generazione, con particolare riguardo al ruolo pro-apoptotico svolto da questo steroide su linfociti di sangue periferico di pazienti asmatici. (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Pirazzoli A.:Glaxo-smithkline- Verona-Italy, Todaro M. e Stassi G.:Dipartimento di Chirurgia e Scienze anatomiche ed Oncologiche umane- Sezione di Anatomia, Università degli Studi di Palermo; Vignola AM: Istituto di Medicina Generale e Pneumologia-Università degli Studi di Palermo - Responsabile Sezione IFC-IBIM-CNR (literal)
Titolo
  • Fluticasone induces apoptosis in peripheral T-lymphocytes: a comparison between asthmatic and normal subjects (literal)
Abstract
  • Apoptosis is an important mechanism allowing inflammation to be limited. Glucocorticoids are the most effective anti-inflammatory agents in asthma therapy and induce cell apoptosis. Since T-lymphocytes are critically involved in airway inflammation in asthma, the effects of fluticasone propionate (FP) on apoptosis in unstimulated and in interleukin (IL)-2 stimulated peripheral blood T-lymphocytes (PBTs) isolated from 14 normal and 19 mild-to-moderate asthmatic subjects were evaluated. Apoptosis was evaluated by: deoxyribonucleic acid (DNA) fragmentation electrophoresis, DNA content, annexin V binding, apoptosis related markers (Fas, B-cell lymphona leukaemia-2 (Bcl-2), Bax, and CD25), and by electron microscopy. FP induced apoptosis in unstimulated PBTs of normal and asthmatic subjects in a time-dependent fashion. In asthma, this effect was associated with a significant decrease of Bcl-2 expression, and with an increase of Bax/Bcl-2 ratio. In PBTs of asthmatics, FP also reduced Fas and CD25 expression. Moreover, in IL-2-stimulated PBTs from both asthmatics and normal subjects, FP was able to induce apoptosis and to reduce Bcl-2, Fas and CD25 expression, whereas negligible effects were detected on Bax expression. This study shows that the glucocorticosteroid, fluticasone, increases apoptosis and modulates expression of apoptosis-related markers in unstimulated and in interleukin-2 stimulated T-lymphocytes. This points towards a potential mechanism by which fluticasone exerts its anti-inflammatory effects. (literal)
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