Altered surfactant protein-A expression in type II pneumocytes in COPD.
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.
Vlachaki
Eleni M
EM
Department of Thoracic Medicine, University Hospital of Heraklion, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
Koutsopoulos
Anastassios V
AV
Tzanakis
Nikolaos
N
Neofytou
Eirini
E
Siganaki
Marianna
M
Drositis
Ioannis
I
Moniakis
Andreas
A
Schiza
Sophia
S
Siafakas
Nikolaos M
NM
Tzortzaki
Eleni G
EG
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*
D015415:Biomarkers; D037662:Pulmonary Surfactant-Associated Protein A