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Original Research: COPD |

Altered Surfactant Protein-A Expression in Type II Pneumocytes in COPD

Eleni M. Vlachaki, MD; Anastassios V. Koutsopoulos, MD, PhD; Nikolaos Tzanakis, MD, PhD; Eirini Neofytou, MSc; Marianna Siganaki, MD; Ioannis Drositis, MD; Andreas Moniakis, MD; Sophia Schiza, MD, PhD; Nikolaos M. Siafakas, MD, PhD, FCCP; Eleni G. Tzortzaki, MD, PhD, FCCP
Author and Funding Information

From the Department of Thoracic Medicine (Drs Vlachaki, Tzanakis, Neofytou, Schiza, Siafakas, and Tzortzaki, and Ms Siganaki), the Department of Pathology (Dr Koutsopoulos), and the Department of Thoracic Surgery (Drs Drositis and Moniakis), University Hospital of Heraklion, Medical School, University of Crete, Greece.

Correspondence to: Eleni Tzortzaki, MD, PhD, FCCP, Department of Thoracic Medicine, University Hospital of Heraklion, Medical School, University of Crete, 71110 Heraklion, Crete, Greece; e-mail: tzortzaki@med.uoc.gr


Part of this article has been presented in abstract form (Vlachaki E, Tzortzaki EG, Koutsopoulos A, et al. Proc Am Thorac Soc. 2006:A624).

Funding/Support: The present study was supported by a Grant of Hellenic Thoracic Society.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(1):37-45. doi:10.1378/chest.09-1029
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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 FEV1 (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 (FEV1, % 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.

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