Document Detail

Altered surfactant protein-A expression in type II pneumocytes in COPD.
MedLine Citation:
PMID:  19741063     Owner:  NLM     Status:  MEDLINE    
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.
Eleni M Vlachaki; Anastassios V Koutsopoulos; Nikolaos Tzanakis; Eirini Neofytou; Marianna Siganaki; Ioannis Drositis; Andreas Moniakis; Sophia Schiza; Nikolaos M Siafakas; Eleni G Tzortzaki
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-09-09
Journal Detail:
Title:  Chest     Volume:  137     ISSN:  1931-3543     ISO Abbreviation:  Chest     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2010-01-06     Completed Date:  2010-02-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0231335     Medline TA:  Chest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  37-45     Citation Subset:  AIM; IM    
Department of Thoracic Medicine, University Hospital of Heraklion, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
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MeSH Terms
Biological Markers / metabolism
Blotting, Western
Disease Progression
Middle Aged
Pneumocytes / metabolism*,  pathology
Pulmonary Disease, Chronic Obstructive / metabolism*,  pathology,  surgery
Pulmonary Surfactant-Associated Protein A / biosynthesis*
Reg. No./Substance:
0/Biological Markers; 0/Pulmonary Surfactant-Associated Protein A

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