Abstract: COPD is characterized by loss of elastic fibers from
small airways and alveolar walls, with the decrease in elastin
increasing with disease severity. It is unclear why there is a lack of
repair of elastic fibers. We have examined fibroblasts cultured from
lung tissue from normal and COPD subjects to determine if the
secretory profile explains lack of tissue repair. In this study,
fibroblasts were cultured from lung parenchyma of bronchial
carcinoma patients with varying degrees of COPD; controls
(non-COPD, n=5), mild COPD (GOLD 1, n=5) and moderate-severe
COPD (GOLD 2-3, n=12). Measurements were made of proliferation,
senescence-associated beta-galactosidase-1, mRNA expression of
IL-6, IL-8, MMP-1, tropoelastin and versican, and protein levels for
IL-6, IL-8, PGE2, tropoelastin, insoluble elastin, and versican. It was
found that GOLD 2-3 fibroblasts proliferated more slowly (p