Exercise Inhibits the Effects of Smoke-Induced COPD Involving Modulation of STAT3

Evaluate the participation of STAT3 in the effects of aerobic exercise (AE) in a model of smoke-induced COPD.

C57Bl/6 male mice were divided into control, Exe, COPD, and COPD+Exe groups. Smoke were administered during 90 days. Treadmill aerobic training begun on day 61 until day 90. Pulmonary inflammation, systemic inflammation, the level of lung emphysema, and the airway remodeling were evaluated. Analysis of integral and phosphorylated expression of STAT3 by airway epithelial cells, peribronchial leukocytes, and parenchymal leukocytes was performed.

AE inhibited smoke-induced accumulation of total cells (p < 0.001), lymphocytes (p < 0.001), and neutrophils (p < 0.001) in BAL, as well as BAL levels of IL-1β (p < 0.001), CXCL1 (p < 0.001), IL-17 (p < 0.001), and TNF-α (p < 0.05), while increased the levels of IL-10 (p < 0.001). AE also inhibited smoke-induced increases in total leukocytes (p < 0.001), neutrophils (p < 0.05), lymphocytes (p < 0.001), and monocytes (p < 0.01) in blood, as well as serum levels of IL-1β (p < 0.01), CXCL1 (p < 0.01), IL-17 (p < 0.05), and TNF-α (p < 0.01), while increased the levels of IL-10 (p < 0.001). AE reduced smoke-induced emphysema (p < 0.001) and collagen fiber accumulation in the airways (p < 0.001). AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells (p < 0.001), peribronchial leukocytes (p < 0.001), and parenchymal leukocytes (p < 0.001).

AE reduces smoke-induced COPD phenotype involving STAT3.