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

¹ Istituto di Fisiopatologia Respiratoria, Consiglio Nazionale delle Ricerche, Palermo, ² Glaxo Wellcome, Verona, ³ Dept of Surgical, Anatomical and Oncological Sciences Human Anatomy Section, Università degli Studi, Palermo, and ⁴ Istituto di Medicina Generale e Pneumologia, Università degli Studi, Palermo, Italy

CORRESPONDENCE: M. Melis, Istituto di Fisiopatologia Respiratoria, Consiglio Nazionale delle Ricerche, Via Trabucco, 180-90146, Palermo, Italy. Fax: 39 0916882165. E-mail: melis@ifr.pa.cnr.it

Keywords: apoptosis, asthma, fluticasone propionate, inflammation

Received: April 23, 2001
Accepted September 5, 2001

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.

This article has been cited by other articles:

				S O'Sullivan, L Cormican, C M Burke, and L W Poulter Fluticasone induces T cell apoptosis in the bronchial wall of mild to moderate asthmatics Thorax, August 1, 2004; 59(8): 657 - 661. [Abstract] [Full Text] [PDF]