Abstract
Although the positive effects of recombinant fibroblast growth factor-2 (rFGF-2) in chronic obstructive pulmonary disease (COPD) have been implicated in previous studies, knowledge of its role in COPD remains limited. The mechanism of FGF2 in a COPD mouse model and the therapeutic potential of rFGF-2 were investigated in COPD. The mechanism and protective effects of rFGF-2 were evaluated in cigarette smoke-exposed or elastase-induced COPD animal models. Inflammation was assessed in alveolar cells and lung tissues from mice. FGF-2 was decreased in the lungs of cigarette smoke-exposed mice. Intranasal use of rFGF-2 significantly reduced macrophage-dominant inflammation and alveolar destruction in the lungs. In the elastase-induced emphysema model, rFGF-2 improved regeneration of the lungs. In humans, plasma FGF-2 was decreased significantly in COPD compared with normal subjects (10 subjects, P = 0.037). The safety and efficacy of inhaled rFGF-2 use was examined in COPD patients, along with changes in respiratory symptoms and pulmonary function. A 2-week treatment with inhaled rFGF-2 in COPD (n = 6) resulted in significantly improved respiratory symptoms compared with baseline levels (P < 0.05); however, the results were not significant compared with the placebo. The pulmonary function test results of COPD improved numerically compared with those in the placebo, but the difference was not statistically significant. No serious adverse events occurred during treatment with inhaled rFGF-2. The loss of FGF-2 production is an important mechanism in the development of COPD. Inhaling rFGF-2 may be a new therapeutic option for patients with COPD because rFGF-2 decreases inflammation in lungs exposed to cigarette smoke.
Highlights
Chronic obstructive pulmonary disease (COPD) is a disease entity that is physiologically characterized by chronic irreversible airflow limitation causing progressive decline of lung function and intermittent episodes of Official journal of the Korean Society for Biochemistry and Molecular BiologyKim et al Experimental & Molecular Medicine (2018) 50:150 term use of corticosteroids can cause complications in patients with advanced stage COPD2,3.The exact mechanism that leads to the presence of pulmonary emphysema, an important part of COPD, is not fully understood
To determine the effects of a decreased Fibroblast growth factors (FGFs)-2 level on the lungs after short-term exposure to cigarette smoke, Bronchoalveolar lavage (BAL) fluid and lung tissue were collected on day 5 from C57BL/6 mice exposed to cigarette smoke for 4 days, and inflammation and the emphysema index representing the COPD patient’s phenotype were determined
The mean linear intercept (MLI) was measured using hematoxylin and eosin (H&E)-stained lung tissue to determine the index of alveolar destruction, which was significantly increased in smoke-exposed mice compared with that in normal air-exposed mice (Fig. 2b)
Summary
The exact mechanism that leads to the presence of pulmonary emphysema, an important part of COPD, is not fully understood. It has been shown that emphysema might be the result of interactions between environmental triggers (such as cigarette smoking) in patients with genetic predisposition. Smoking is known as the main cause of the development of emphysema[4]. In the case of emphysema, oxidative stress mainly caused by cigarette smoking results in the development of cellular injury and apoptosis[6]. TGF is known as a major regulator of fibrosis, it has recently been found to play a significant role in the development of emphysema[7]. FGF-2 is a downstream mediator of TGF-β and is important in wound healing[9]
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