title: Altered surfactant protein-A expression in type II pneumocytes in COPD.
abstract: BACKGROUND
  Pulmonary surfactant protein A (SP-A) is a lectin, with multiple functions that contribute to innate host defense and the regulation of the inflammatory process in the lung. In normal conditions, SP-A seems to protect against the effects of smoking. However, studies in smokers with or without COPD are limited.
  
  
  METHODS
  Western blots on lung tissue specimens from 60 male subjects (32 patients with COPD, 18 smokers without COPD, and 10 control nonsmokers) for SP-A and the housekeeping protein actin were carried out. Additionally, the SP-A expression pattern was evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded lung tissue sections from the same subjects.
  
  
  RESULTS
  Western blots revealed significantly higher SP-A levels in control nonsmokers (4.8 +/- 0.05) when compared with patients with COPD (0.6 +/- 0.7) and smokers without COPD (2.4 +/- 0.9), (P < .05). However, differences that were not statistically significant were observed in SP-A levels among the patients with COPD and the smokers without COPD (P = .12). The immunohistochemical examinations showed an increase in the overall number of type II pneumocytes per high-power field in patients with COPD, but a decreased ratio of SP-A positive type II pneumocytes to total type II pneumocytes, compared with smokers without COPD (P = .001). This ratio was also correlated with FEV(1) (percent predicted [% pred]), (r = 0.490, P = .001). The overall number of alveolar macrophages per high-power field was significantly higher in patients with COPD compared with smokers without COPD (P = .001). The ratio of SP-A positive alveolar macrophages was increased in patients with COPD when compared with smokers without COPD (P = .002), while this was correlated with airway obstruction (FEV(1), % pred) (r = 0.281, P = .04).
  
  
  CONCLUSIONS
  Our results indicate that altered SP-A expression could be another link to COPD pathogenesis and highlights the need for further studies on surfactant markers in COPD.
authors.affiliation: Department of Thoracic Medicine, University Hospital of Heraklion, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
authors.forename: Eleni M
authors.initials: EM
authors.lastname: Vlachaki
authors.forename: Anastassios V
authors.initials: AV
authors.lastname: Koutsopoulos
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Tzanakis
authors.forename: Eirini
authors.initials: E
authors.lastname: Neofytou
authors.forename: Marianna
authors.initials: M
authors.lastname: Siganaki
authors.forename: Ioannis
authors.initials: I
authors.lastname: Drositis
authors.forename: Andreas
authors.initials: A
authors.lastname: Moniakis
authors.forename: Sophia
authors.initials: S
authors.lastname: Schiza
authors.forename: Nikolaos M
authors.initials: NM
authors.lastname: Siafakas
authors.forename: Eleni G
authors.initials: EG
authors.lastname: Tzortzaki
mesh_terms: D056809:Alveolar Epithelial Cells / Q000378:metabolism* / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D018450:Disease Progression; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011013:Pneumonectomy; D011379:Prognosis; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D037662:Pulmonary Surfactant-Associated Protein A / Q000096:biosynthesis*
chemical_list: D015415:Biomarkers; D037662:Pulmonary Surfactant-Associated Protein A