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Published ahead of print on February 15, 2007, doi:10.1164/rccm.200607-908OC
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American Journal of Respiratory and Critical Care Medicine Vol 175. pp. 919-925, (2007)
© 2007 American Thoracic Society
doi: 10.1164/rccm.200607-908OC

Original Article

Cigarette Smoking Alters Bronchial Mucosal Immunity in Asthma

Maria Tsoumakidou1,2, William Elston1,3, Jie Zhu1, Zhuo Wang1, Elizabeth Gamble4, Nikos M. Siafakas2, Neil C. Barnes3 and Peter K. Jeffery1

1 Lung Pathology Unit, Department of Gene Therapy, Imperial College London, London, United Kingdom; 2 Thoracic Medicine, Department of Internal Medicine, University of Crete, Heraklion, Greece; 3 Respiratory Medicine, St Barts and the London Hospital Trust, London, United Kingdom; and 4 Respiratory Medicine, Bristol Royal Infirmary, Bristol, United Kingdom

Correspondence and requests for reprints should be addressed to Peter K. Jeffery, FRCPath., D.Sc., Lung Pathology, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK. E-mail: p.jeffery{at}imperial.ac.uk

Rationale: Cigarette smoking worsens asthma and is associated with reduced response to corticosteroid therapy. As cigarette smoke is known to have immunomodulatory effects, we hypothesized that one mechanism by which smoking mediates its adverse effect is by reduction of the numbers of bronchial mucosal dendritic cells (DCs), which control B-cell growth and T-cell responses.

Objectives: We set out to sample the bronchial mucosa in smoking and never-smoking patients with asthma and to count DCs, B cells, and cells expressing genes for two key T-lymphocyte regulatory cytokines.

Methods: Twenty-one never-smoker patients with asthma (6 steroid naive), 24 smoker patients with asthma (9 steroid naive), and 10 healthy never-smokers (control subjects) were recruited and their endobronchial biopsy samples were immunostained for detection of mature DCs (CD83+), Langerhans cells (CD1a+), B lymphocytes (CD20+), and helper T-cell type 1 (IFN-{gamma}) and helper T-cell type 2 (IL-4) cytokine–expressing cells.

Measurements and Main Results: The number (per square millimeter) of CD83+ mature DCs was significantly lower in smoker patients with asthma (median [range]: 37 [0, 131]) in comparison with never-smoker steroid-naive and steroid-treated patients with asthma (76 [24, 464]; p = 0.006) or control subjects (85 [40, 294]; p = 0.004). Moreover, B cells were fewer in smoker (26 [4, 234]) versus never-smoker steroid-naive and steroid-treated patients with asthma (45 [10, 447]; p = 0.01) and in smoker steroid-naive patients with asthma (23 [4, 111]) versus control subjects (34 [10, 130]; p = 0.05). The number of cells expressing IFN-{gamma} showed a trend toward fewer in smoker (70 [6, 24]) versus never-smoker steroid-naive patients with asthma (144 [44, 323]; p = 0.10).

Conclusions: There are important and statistically significant differences in the number of CD83+ mature DCs and B cells in the large airways of smokers with asthma. We speculate that their reductions may render patients with asthma less responsive to corticosteroids and more susceptible to infection.

Key Words: asthmatic • smoker • inflammation • dendritic cells • lymphocytes


AT A GLANCE COMMENTARY

Scientific Knowledge on the Subject
Smoking may worsen asthma and render it less responsive to the beneficial effects of inhaled steroid therapy. Cigarette smoke impairs the function of dendritic cells and alters their number.

What This Study Adds to the Field
One mechanism by which smoking mediates its adverse effects in asthma is by reduction of the numbers of bronchial mucosal dendritic cells.

 



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