title: Increased intraepithelial T-cells in stable COPD.
abstract: BACKGROUND
  The airway epithelium is the first line of defence in the response to inhaled particles and irritants. Chronic obstructive pulmonary disease (COPD) is an inflammatory disease characterised by an irreversible loss of lung function, with cigarette smoking as a major risk factor. Here, we address intraepithelial T-cells in COPD, as these cells are a distinct T-cell subtype thought to have important regulatory functions. We hypothesised that intraepithelial T-cells play a role in the response to lung irritants and that the T-cell populations would be altered and associated with signs of inflammation in COPD.
  
  
  METHODS
  Bronchoscopy with endobronchial mucosal biopsy sampling was performed in 22 patients (mean age; 57) with stable COPD (median FEV(1)% predicted: 51). Age- and smoking- matched smokers (S) with normal lung function (n=14) and age-matched non-smokers (NS) (n=15) served as controls. Airway inflammation was recorded visually using bronchitis index (BI). Biopsy specimens were processed into glycol methacrylate resin and inflammatory cells were stained immunohistochemically.
  
  
  RESULTS
  The number of intraepithelial CD4+ T-cells were significantly higher in COPD patients compared to smokers as well as trend towards significance in non-smokers (p=0.005 and p=0.036, respectively), whereas intraepithelial CD8+ T-cells number were increased in patients with COPD compared to non-smokers (p=0.017). Both patients with COPD and smokers had a higher BI than non-smokers (p<0.001 for both).
  
  
  CONCLUSIONS
  The present data suggest a role for intraepithelial CD4+ and CD8+ T-cells in stable COPD and indicate that T-cells are of importance in the long-term inflammatory response in COPD or, alternatively, play a regulatory role.
authors.affiliation: Department of Medicine, Division of Respiratory Medicine, Karolinska Institutet, Solna, Stockholm, Sweden. magnus.lofdahl@karolinska.se
authors.forename: Magnus J
authors.initials: MJ
authors.lastname: Löfdahl
authors.forename: Ester
authors.initials: E
authors.lastname: Roos-Engstrand
authors.forename: Jamshid
authors.initials: J
authors.lastname: Pourazar
authors.forename: Anders
authors.initials: A
authors.lastname: Bucht
authors.forename: Barbro
authors.initials: B
authors.lastname: Dahlen
authors.forename: Göran
authors.initials: G
authors.lastname: Elmberger
authors.forename: Anders
authors.initials: A
authors.lastname: Blomberg
authors.forename: C Magnus
authors.initials: CM
authors.lastname: Sköld
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy; D001980:Bronchi / Q000276:immunology / Q000473:pathology; D001991:Bronchitis / Q000276:immunology / Q000473:pathology; D001999:Bronchoscopy; D004847:Epithelial Cells / Q000276:immunology / Q000473:pathology; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology* / Q000473:pathology; D020545:Respiratory Mucosa / Q000276:immunology* / Q000473:pathology; D012720:Severity of Illness Index; D012907:Smoking / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014797:Vital Capacity