title: Tenascin-C and alpha-smooth muscle actin positive cells are increased in the large airways in patients with COPD.
abstract: BACKGROUND
  Chronic obstructive pulmonary disease (COPD) is characterized by inflammation and remodeling of the lungs. This results in alterations in extracellular matrix (ECM) and structural changes leading to airflow obstruction. We studied the expression of tenascin-C (Tn-C) and alpha smooth muscle actin (α-SMA), which act as a marker of myofibroblasts, in large airways from COPD patients. Our aim was to elucidate whether this expression correlated with smoking or with disease development.
  
  
  METHODS
  Bronchoscopy was performed on 20 COPD patients (mean age 56 years; range 39-61; FEV1/FVC < 70% and FEV1 median 53% (range 33-69) of predicted). Age and smoking matched smokers (S) without COPD (n = 13) and age matched non-smokers (NS) (n = 14) served as controls. Bronchial mucosal biopsies were analyzed by immunohistochemistry. The distribution of Tn-C expression was assessed and graded in three levels, and the number of spindle shaped cells staining positive for α-SMA were counted.
  
  
  RESULTS
  Biopsies from COPD patients had more (P < 0.001) Tn-C expression than the two control groups. A significantly (P < 0.05) increased number of spindle shaped cells expressing α-SMA was observed in COPD patients compared with the controls. Smokers and nonsmokers did not differ in this respect. The expression of Tn-C correlated positively (P < 0.001) to the number of α-SMA positive cells.
  
  
  CONCLUSIONS
  We demonstrate increased expression of Tn-C and α-SMA positive cells in the large airways in COPD. This was not associated to smoking per se, but to the presence of airway obstruction. Our findings add new information regarding remodeling characteristics and highlight the large airways as a potential site for airways obstruction in COPD.
authors.affiliation: Dept. of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm Sweden. magnus.lofdahl@karolinska.se
authors.forename: Magnus
authors.initials: M
authors.lastname: Löfdahl
authors.forename: Riitta
authors.initials: R
authors.lastname: Kaarteenaho
authors.forename: Elisa
authors.initials: E
authors.lastname: Lappi-Blanco
authors.forename: Göran
authors.initials: G
authors.lastname: Tornling
authors.forename: Magnus C
authors.initials: MC
authors.lastname: Sköld
mesh_terms: D000199:Actins / Q000032:analysis*; D000328:Adult; D000704:Analysis of Variance; D001706:Biopsy; D001980:Bronchi / Q000737:chemistry* / Q000503:physiopathology; D001999:Bronchoscopy; D016022:Case-Control Studies; D003893:Desmin / Q000032:analysis; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D020545:Respiratory Mucosa / Q000737:chemistry*; D012907:Smoking / Q000009:adverse effects; D013548:Sweden; D019063:Tenascin / Q000032:analysis*; D015854:Up-Regulation; D014746:Vimentin / Q000032:analysis; D014797:Vital Capacity
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D003893:Desmin; D019063:Tenascin; D014746:Vimentin