Abstract
Acute respiratory dystress syndrome (ARDS) is characterized by respiratory insufficiency, severe inflammation, disruption of alveolar-capillary membrane, resulting in edema and hypoxemia. Aerobic exercise (AE) of mild to moderate intensity has already been shown to have beneficial effects on the immune system, with direct impact on lung diseases. This study investigated the role of IL-10 and TLR-4 in the anti-inflammatory effects of AE in a model of pulmonary and extrapulmonary LPS-induced ARDS. C57Bl/6 mice were distributed into 6 experimental groups (n=10/group): Control, AE, LPS i.t., LPS i.p., AE+LPS i.t., Exercise+LPS i.p. Moderate intensity AE was performed in treadmill for 5 weeks, 4x/week, 1h/session. 24 hours after the last AE session, each animal received intratracheal (i.t) administration of LPS (10μg) or administration of intraperitoneal (i.p.) of LPS (100μg) and after 24 hours the animals were euthanized. AE reduced both LPS i.t. and LPS i.p induce neutrophils accumulation in lung parenchyma (p<0.01) and in BAL (p<0.01). AE also attenuated the serum and BAL levels of IL-1beta, IL-6, CXCL1/KC, TNF-alpha and IFN-gamma (p<0.05), evaluated by ELISA. AE increased the serum and BAL levels of IL-10 (p<0.05). AE also reduced the expression of TLR-4 in the lung homogenates, evaluated by western blotting (p<0.05). We conclude that AE reducesd the impact of LPS-induced ARDS independent of the etiology and such effects seems to be mediated by the modulation of AE on the secretion of anti-inflammatory cytokine IL-10 and on the TLR-4.
- © 2014 ERS
