Airway mucosal inflammation in COPD is similar in smokers and ex-smokers: a pooled analysis

¹ Dept of Respiratory Medicine, London Chest Hospital, UK; and Lung Pathology, Imperial College London at the Royal Brompton Hospital, London, UK
² Dept of Pulmonology, Leiden University Medical Centre, Leiden, The Netherlands
³ Dept of Respiratory Medicine, London Chest Hospital, UK
⁴ Dept of Respiratory Medicine, Newham University Hospital NHS Trust, UK
⁵ Massey University School of Health Sciences, Auckland, New Zealand
⁶ Lung Pathology, Imperial College London at the Royal Brompton Hospital, London, UK
⁷ Instituto di Fisiopatologia Respiratoria, Palermo, Italy
⁸ Dept of Pneumology and Allergy, University Medical Clinic, Jena, Germany
⁹ Servei de Pneumologia, Clinica Tres Torres, Hospital Vall d'Hebron, Barcelona
¹⁰ Dept of Respiratory Medicine, Glenfield Hospital, Leicester, UK

^* To whom correspondence should be addressed. E-mail: neil.barnes{at}bartsandthelondon.nhs.uk.

	Abstract

Bronchial biopsies in COPD demonstrate increased numbers of CD8+ T-lymphocytes, macrophages and, in some studies, neutrophils and eosinophils. Smoking cessation affects the rate of FEV₁ decline in COPD, but the effect on inflammation is uncertain. We have compared bronchial biopsy inflammatory cell counts in current and ex-smokers with COPD.

We performed a pooled analysis of data for subepithelial inflammatory cell counts from three bronchial biopsy studies that included COPD patients who were either current smokers or ex-smokers.

In total, cell count data from 101 subjects; 65 current smokers and 36 ex-smokers were analysed for the following cell types: CD4+ and CD8+ T-lymphocytes, CD68+ (monocytes/macrophages), neutrophil elastase+ (neutrophils), EG2+ (eosinophils), mast cell tryptase and cells mRNA positive for TNF. Current smokers and ex-smokers were similar in terms of lung function as measured by FEV₁% predicted, FVC and FEV₁/FVC. The results demonstrate that there were no statistically significant differences between smokers and ex-smokers in the numbers of any of the inflammatory cell types or markers analysed.

We conclude that in established COPD, bronchial mucosal inflammatory cell infiltrate is similar in ex-smokers and those that continue to smoke.

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