http://www.cnr.it/ontology/cnr/individuo/prodotto/ID168849
Fluticasone induces apoptosis in peripheral T-lymphocytes: a comparison between asthmatic and normal subjects (Articolo in rivista)
- Type
- Label
- 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)
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- Pagina fine
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- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- Impact Factor: 2.989 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto
- 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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