Inflammation in bronchial biopsies of subjects with chronic bronchitis: inverse relationship of CD8+ T lymphocytes with FEV1.
In order to determine whether the airway inflammatory cells of chronic obstructive pulmonary disease (COPD) are different from those seen in asthma, we have studied a subepithelial zone, 100 microns deep to the epithelial reticular basement membrane in bronchial biopsies taken from five normal nonsmoking subjects without chronic bronchitis or asthma (FEV1 percentage of predicted [mean +/- SD] 105.7 +/- 25.3), 11 subjects with chronic bronchitis alone (FEV1 percentage of predicted 98.5 +/- 12.9), and 13 subjects with chronic bronchitis in whom there was also evidence of airflow limitation (i.e., COPD; FEV1 percentage of predicted 59.7 +/- 10.0). Using immunohistochemical markers, we counted distinct types of inflammatory cell and expressed them as [median and range] per mm basement membrane. When there was airflow limitation we found significantly increased numbers of CD3+ T lymphocytes (COPD 22.3 [2.6 to 68.2] versus normal 3.7 [1.5 to 16.3]; p < 0.05), an increased number of CD8+ cells (COPD 19.3 [1.8 to 45.5] versus normal 2.3 [0.9 to 4.2]; p < 0.01), and increased expression of HLA-DR (COPD versus normal; p = 0.01). There was also an increased number of CD68+ cells (i.e., macrophages) (COPD 7.4 [0.4 to 16.9] versus normal 0.7 [0 to 2.6]; p < 0.01; COPD versus chronic bronchitis alone 2.7 [0 to 12.8]; p < 0.05). There were no significant differences between the groups in the numbers of subepithelial neutrophils, mast cells, eosinophils or B lymphocytes. There were weak but significant negative associations between the CD8+ T-cell subset (r = -0.42), neutrophils (r = -0.46), and eosinophils (r = -0.53) and FEV1 percentage of predicted in all the chronic bronchitic smokers (p < 0.05). The data confirm the involvement of subepithelial T lymphocytes and macrophages in smoking-induced airflow limitation and provide novel data which support the view that COPD is distinct from asthma with respect to the predominance of the CD8+ T-cell subset in this smoking-related condition.
O'Shaughnessy
T C
TC
Lung Pathology Unit, Imperial College, London, United Kingdom.
Ansari
T W
TW
Barnes
N C
NC
Jeffery
P K
PK
D000328:Adult; D001249:Asthma / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D001706:Biopsy; D001980:Bronchi / Q000276:immunology / Q000473:pathology*; D001991:Bronchitis / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D001999:Bronchoscopy; D016827:CD8 Antigens / Q000032:analysis*; D002452:Cell Count; D002908:Chronic Disease; D004848:Epithelium / Q000473:pathology; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D016130:Immunophenotyping; D008173:Lung Diseases, Obstructive / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012907:Smoking / Q000276:immunology / Q000503:physiopathology
D016827:CD8 Antigens