Abstract
Introduction Moderate aerobic exercise training accelerates the resolution of lung fibrosis in a model of bleomycin-induced pulmonary fibrosis. However, whether it can inhibit the development of lung fibrosis is unknown. Materials and Methods C57Bl/6 mice were distributed into four groups: Control (Co), Exercise (Exe), Bleomycin (Bleo), and Bleomycin+Exercise (Bleo+Exe). A single bleomycin dose (1.5 UI/kg) was administered orotracheally and treadmill exercise started in the same day, enduring for 4 weeks, 5x/week, 60 minutes/session, at moderate intensity. Lung mechanics, systemic and pulmonary inflammation, and lung remodeling were evaluated. Lung homogenates were used to evaluate the antioxidant status. Results Total cells, macrophages, lymphocytes, and neutrophils numbers, in agreement with IL-6 levels, were higher in the BAL and serum of Bleo group, compared to other groups. In addition, lung levels of LTB4 in Bleo were higher than other groups, whereas SOD activity and nitric oxide levels in exercised groups (Exe and Exe+Bleo) compared to the Bleo group. Lung GPX activity was lower in Bleo and Exe+Bleo groups compared to others. Exe and Exe+Bleo groups also showed higher IL-10 expression by lung macrophages than other groups, whereas TGF-β expression was higher in Exe, Bleo, and Exe+Bleo groups compared to control. CCR7 expression was induced only in the Exe group. However, exercise did not improve lung remodeling and mechanics, or serum and pulmonary levels of VEGF, IGF-1, and TGF-β. Conclusion Aerobic exercise training initiated concomitantly with induction of pulmonary fibrosis reduces lung and systemic inflammation but fails to inhibit lung fibrosis and mechanics impairment.
Highlights
Moderate aerobic exercise training accelerates the resolution of lung fibrosis in a model of bleomycin-induced pulmonary fibrosis
VEGF levels (Figure 1(f)) in the Bronchoalveolar Lavage (BAL) of the Bleo group were significantly higher than Co (p < 0:001) and Exe (p < 0:01) groups, VEGF levels in the Exe+Bleo group were only higher than Co (p < 0:05)
Our findings here demonstrate that, even though the exercise training was not able to alter the collagen deposition in the parenchyma or even some key pulmonary mechanic parameters, the aerobic exercise training putatively reduced the recruitment of immune system cells, the release of proinflammatory mediators/cytokines both in the lung and blood, and increased the IL-10 expression by lung macrophages of mice submitted to an experimental model of bleomycin-induced lung fibrosis
Summary
Moderate aerobic exercise training accelerates the resolution of lung fibrosis in a model of bleomycin-induced pulmonary fibrosis. Whether it can inhibit the development of lung fibrosis is unknown. There is no curative treatment for IPF, and many studies emerged to ensure the survival and improve the quality of life of these patients, by preserving lung function and minimizing adverse effects of therapy [1,2,3]. Monitored physical exercise in individuals with IPF reduces dyspnea incidence, improves exercise performance (distance covered, effort tolerance, and aerobic capacity), and brings many health benefits, such as higher quality of life and lower symptoms of disease [4,5,6,7]. There is scarce information on the mechanisms by which exercise ameliorates IPF condition, since only few preclinical studies shed some light in the cellular and molecular events associated [8, 9]
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