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Interleukin-5 inhibits glucocorticoid-mediated apoptosis in human eosinophils
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  1. Sven Brode,
  2. Neda Farahi,
  3. Andrew S Cowburn,
  4. Jatinder K Juss,
  5. Alison M Condliffe,
  6. Edwin R Chilvers
  1. Respiratory Medicine Division, Department of Medicine, University of Cambridge, Cambridge, UK
  1. Correspondence to Professor Edwin R Chilvers, Department of Medicine, University of Cambridge, Box 157, Addenbrooke's Hospital, CUHNHSFT, Hills Road, Cambridge CB2 OQQ, UK; erc24{at}cam.ac.uk

https://doi.org/10.1136/thx.2009.124909

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    Glucocorticoids (GCs) represent one of the most effective treatments for eosinophil-mediated inflammatory diseases such as asthma. GCs act through the GC receptor, leading to proinflammatory cytokine suppression and a reduction in the number of inflammatory cells including eosinophils and T cells.1 However, the benefits of GCs have been limited by their side effects and the presence of GC resistance. This led to the development of more selective GCs such as fluticasone propionate (FP) and fluticasone furoate (FF).2

    Increased eosinophil survival has been proposed as a mechanism underlying tissue eosinophilia, and part of the anti-inflammatory effects of GCs has been attributed to their ability to promote eosinophil apoptosis. Interleukin 5 (IL-5) enhances eosinophil survival by inhibiting apoptosis, and increased IL-5 expression is reported in eosinophilic inflammation.3 We sought to address the ability of the ‘enhanced-affinity’ FF, alongside dexamethasone (DEX) and FP, to modulate eosinophil apoptosis and their potential to …

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