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Sputum IL-6 concentrations in severe asthma and its relationship with FEV1
  1. J B Morjaria1,
  2. K S Babu1,
  3. P Vijayanand1,
  4. A J Chauhan2,
  5. D E Davies1,
  6. S T Holgate1
  1. 1Infection, Inflammation and Immunity, Southampton University Hospitals Trust, Southampton, UK
  2. 2Department of Respiratory Medicine, Queen Alexandra Hospital, Portsmouth, UK
  1. Correspondence to Dr J B Morjaria, Mailpoint 810, South Academic Block, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK; jbm{at}

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As asthma becomes more severe it adopts additional characteristics including corticosteroid refractoriness and a neutrophil-predominant inflammatory response implicating Th1 or Th17 responses involving cytokines such as tumour necrosis factor α, interleukin (IL)-6 and IL-8. We have examined the role of IL-6 and IL-8 in severe asthma. Subjects with severe asthma (GINA stage IV) who were exacerbation-free for ≥4 weeks with a forced expiratory volume in 1 s (FEV1) >30% but <80% predicted were studied from the baseline parameters of a clinical trial.1 Cell counts and cytokines were measured in induced sputum (see online supplement for Methods).

Eighteen subjects (9M, 9F) with severe asthma (mean±SD age 43.4±11.4 years (1SD), FEV1 59±14% predicted) were studied (see table 1 in online appendix). The median (IQR) levels of sputum IL-8, IL-6, neutrophils (%), macrophages (%) and eosinophils (%) were 1853.8 pg/ml (1376.8–2537.7), 70.0 pg/ml (28.55–127.5), 32.5% (24.1–42.6), 46.8% (39.8–54.8) and 4.4% (3.2–9.4), respectively. We observed significant negative correlations between FEV1 …

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  • Funding This study was supported by an educational grant from Wyeth Pharmaceuticals, UK, who were not sponsors of the study. The study was part of a trial that was investigator-initiated and the sponsors were not involved in the study design, data collection, analysis or interpretation of the data. STH is a UK Medical Research Council funded Clinical Professor.

  • Competing interests This study was conducted with an educational grant from Wyeth Pharmaceuticals. JBM was funded by the educational grant to conduct this study. AJC in the last 8 years has received research funding, honoraria for lectures and educational grants from Astra Zeneca, Glaxo Smith Kline, Boehringer Ingelheim and Merck and has been on Advisory Boards for Astra Zeneca and Glaxo Smith Kline. STH is a consultant for Novartis, Synairgen, Merck, Wyeth and Centocor and has received lecture fees from these companies. The other authors have no competing interests.

  • Ethics approval This study was conducted with the approval of the SE Hampshire and Isle of Wight Research Ethics Committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.