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Airway epithelial inflammatory responses and clinical parameters in COPD

Academic Unit of Respiratory Medicine, St Bartholomew's and the Royal London Hospital School of Medicine and Dentistry, London, UK

CORRESPONDENCE: J.A. Wedzicha, Academic Unit of Respiratory Medicine, Dominion House, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK. Fax: 44 2076018616. E-mail: j.a.wedzicha@qmul.ac.uk

Keywords: airway, chronic obstructive pulmonary disease, corticosteroids, epithelium, inflammation

Received: October 14, 2002
Accepted March 11, 2003

This study was supported by the Joint Research Board, St Bartholomew's Hospital, London, UK.

This study examined inflammatory responses from primary cultured human bronchial epithelial cells in chronic obstructive pulmonary disease (COPD) and the clinical factors modulating them.

Epithelial cells from bronchoscopic biopsies from 14 patients with COPD ((mean±sd) age 74.6±5.7 yrs, forced expiratory volume in one second (FEV₁) 1.21±0.36 L, FEV₁ % predicted 51.1±15.8%, 51.5±24.0 pack-yrs of smoking, inhaled steroid dosage 1237.5±671.0 µg·day^–1, Medical Research Council (MRC) dyspnoea score 3.18±1.33) and eight current/exsmokers with normal pulmonary function (age 60.4±13.5 yrs, FEV₁ 2.66±1.27 L, FEV₁ % pred 89.6±17.7%, 49±44 pack-yrs of smoking, MRC dyspnoea score 1±0) were grown in primary culture and exposed to 50 ng·mL^–1 tumour necrosis factor-.

Stimulated COPD cells produced significantly more interleukin (IL)-6 at 24 and 48 h, and IL-8 at 6 and 24 h than unstimulated COPD cells. This response was not seen in cells from current/exsmokers. IL-6 and IL-8 production was lower in COPD patients taking inhaled steroids.

Following an inflammatory stimulus, bronchial epithelial cells in chronic obstructive pulmonary disease show a significant cytokine response not seen in smokers with normal pulmonary function and this may be modified by inhaled steroid therapy.

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