Bronchial mucosal dendritic cells in smokers and ex-smokers with COPD: an electron microscopic study.
BACKGROUND
Bronchial mucosal dendritic cells (DCs) initiate and regulate immune responses to inhaled antigens, viruses and bacteria. Currently, little is known of their numbers in patients with chronic obstructive pulmonary disease (COPD). While reductions in their numbers have been reported recently in smokers with asthma, nothing is known of the effects of cigarette smoking on bronchial DCs in COPD. The present study compares DC numbers in smokers and ex-smokers with COPD.


METHODS
Endobronchial biopsies were obtained from 15 patients with moderate to severe COPD (10 current smokers with median forced expiratory volume in 1 s (FEV1) 45.5% predicted (range 23-68) and 5 ex-smokers with median FEV1 30% predicted (range 21-52)), 11 non-smokers with asthma (median FEV1 102% predicted (range 89-116)) and 11 non-smoker healthy controls (median FEV1 110% predicted (range 92-135)). Transmission electron microscopy (TEM) was used to identify the total population of DCs by their ultrastructure and their number in the epithelium and subepithelium was counted.


RESULTS
Median (range) DC numbers were significantly lower in current smokers with COPD in the epithelium (0.0 (0.0-156.8) cells/mm2) and the subepithelium (4.5 (0.0-63.6) cells/mm2) compared with ex-smokers with COPD (97.9 (93.5-170.3) cells/mm2 in the epithelium (p<0.05); 91.8 (38.2-283.3) cells/mm2 in the subepithelium (p<0.01)). DC numbers in ex-smokers with COPD were similar to those in subjects with atopic asthma and healthy controls (131.6 (33.3-235.5) cells/mm2 in the epithelium and 64.4 (0.0-182.4) cells/mm2 in the subepithelium for the latter).


CONCLUSIONS
In COPD, bronchial mucosal DC numbers are lower in current smokers while, in those who quit, numbers are similar to non-smoking subjects with asthma and non-smoking healthy controls. The functional consequences of the reduction in mucosal DC numbers in smokers with COPD have yet to be determined.
Rogers
A V
AV
Lung Pathology Unit, Department of Gene Therapy, Imperial College London, London, UK.
Adelroth
E
E
Hattotuwa
K
K
Dewar
A
A
Jeffery
P K
PK
D000293:Adolescent; D000328:Adult; D000368:Aged; D001249:Asthma / Q000473:pathology; D001707:Biopsy, Needle; D001980:Bronchi / Q000473:pathology / Q000648:ultrastructure*; D001999:Bronchoscopy; D016022:Case-Control Studies; D003713:Dendritic Cells / Q000378:metabolism / Q000648:ultrastructure*; D005260:Female; D006801:Humans; D008297:Male; D046529:Microscopy, Electron, Transmission / Q000592:standards; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000473:pathology*; D020545:Respiratory Mucosa / Q000648:ultrastructure*; D012907:Smoking / Q000009:adverse effects* / Q000473:pathology; D016540:Smoking Cessation