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  1. Fatemeh Fattahi1,2,3,
  2. Franke Volbeda1,3,4,
  3. Martine Broekema2,3,
  4. Monique E Lodewijk2,3,
  5. Machteld N Hylkema2,3,
  6. Helen K Reddel5,
  7. Wim Timens2,3,
  8. Dirkje S Postma1,3,
  9. Nick H T ten Hacken1,3
  1. 1 Department of Pulmonology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  2. 2 Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  3. 3 Groningen Research Institute for Asthma and COPD (GRIAC), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  4. 4 Pulmonary Rehabilitation Centre Beatrixoord, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  5. 5 Woolcock Institute of Medical Research and University of Sydney, Sydney, Australia
  1. Correspondence to Dr Nick H T ten Hacken, Department of Pulmonology, University of Groningen, University Medical Center Groningen, PO Box 30001, Groningen 9700 RB, The Netherlands; n.h.t.ten.hacken{at}umcg.nl

https://doi.org/10.1136/thoraxjnl-2012-203023

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    We have read with great interest the comments by Dr Persson1 on our recent paper in Thorax,2 in which we showed that clinical control of asthma associated significantly with lower numbers of activated eosinophils in the bronchial wall, yet only weakly with sputum eosinophils. As the number of eosinophils in biopsies did not associate with clinical control of asthma, we speculated that activation of eosinophils (measured as eosinophil protein X (EXP)-immunopositive pixels per area) in bronchial biopsies reflects the level of disease control better than the number of eosinophils itself.2 As lysis of activated …

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