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Chest. 2014 Nov;146(5):1159-1165. doi: 10.1378/chest.14-0373.

Simultaneous assessment of hepatocyte growth factor and vascular endothelial growth factor in epithelial lining fluid from patients with COPD.

Author information

1
From the Department of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan. Electronic address: kanazawa-h@med.osaka-cu.ac.jp.
2
From the Department of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.

Abstract

BACKGROUND:

Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are involved in the pathogenesis of various lung diseases. This study was designed to determine the possible interactions of these growth factors in the development of COPD.

METHODS:

We measured the levels of HGF and VEGF in epithelial lining fluid obtained from central or peripheral airways using a bronchoscopic microsampling technique in 10 never smokers, 14 smokers without COPD, and 24 smokers with COPD. We also evaluated whether their levels were correlated with pulmonary function parameters and the grade of low attenuation area (LAA) observed in high-resolution CT scans.

RESULTS:

HGF and VEGF levels in the peripheral airways of smokers with COPD were significantly lower than those in never smokers and smokers without COPD. In smokers with COPD, HGF and VEGF levels of the peripheral airways inversely correlated with the degree of airway obstruction and diffusing capacity of the lung. The HGF and VEGF levels also correlated with the grade of LAA. Although the VEGF levels of smokers with and without COPD overlapped considerably, HGF levels were markedly higher in smokers without COPD.

CONCLUSIONS:

Upregulated HGF probably compensated for the reduced levels of VEGF and preserved the pulmonary function in smokers without COPD. By contrast, both HGF and VEGF levels were decreased in smokers with COPD, which likely led to the development of COPD. Thus, the level of HGF relative to that of VEGF may be a reliable indicator of the risk for COPD.

PMID:
24832895
DOI:
10.1378/chest.14-0373
[Indexed for MEDLINE]

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