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Fluticasone induces T cell apoptosis in the bronchial wall of mild to moderate asthmatics
  1. S O’Sullivan1,
  2. L Cormican2,
  3. C M Burke2,
  4. L W Poulter1
  1. 1Department of Immunology, Royal Free and University College Hospital Medical School, London NW3 2QG, UK
  2. 2Department of Respiratory Medicine, James Connolly Memorial Hospital, Dublin 15, Ireland
  1. Correspondence to:
    Dr S O’Sullivan
    Department of Immunology, Royal Free and University College Hospital Medical School, London NW3 2QG, UK;


Background: Cytokines which signal via the gamma chain of the interleukin (IL)-2 receptor and the interferons (IFNs) have been shown to enhance T cell survival in vitro by rescuing cells from apoptosis.

Methods: A study was undertaken to determine whether treatment with inhaled fluticasone propionate (FP; 250 μg twice daily) for 2 weeks could modulate production of IL-15 or IFN-β and thereby affect T cell survival in bronchial tissue of 10 patients with mild/moderate asthma. Bronchial biopsy specimens were taken before and on completion of treatment.

Results: The mean (95% CI) number of T cells per unit area decreased in the asthmatic group following 2 weeks of treatment with FP (from 7.0 (5.6 to 8.4) to 4.5 (4.0 to 5.1); p = 0.001). There was an increase in the percentage of T cells undergoing apoptosis following FP treatment as assessed by T cell/TUNEL staining (from 4.5 (2.6 to 6.4) to 8.7 (6.6 to 10.8); p = 0.0001). The percentage of cells staining for IL-15 and IFN-β in the lamina propria, determined by an alkaline phosphatase biotin streptavidin technique, decreased significantly from baseline values of 31.6 (23.4 to 39.7) to 19.6 (12.5 to 26.7), p = 0.039 for IL-15 and from 18.9 (13.5 to 24.4) to 9.5 (5.9 to 13.1), p = 0.007 for IFN-β following 2 weeks of treatment with FP. However, only the decrease in the percentage of cells staining for IL-15 was significantly correlated with an increased number of apoptotic T cells following treatment (p = 0.008).

Conclusion: These findings support a novel mechanism for the ability of inhaled corticosteroids to decrease T cell numbers, possibly by downregulation of the cytokine IL-15.

  • apoptosis
  • T cells
  • asthma
  • fluticasone propionate

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