Protective effects of aerobic exercise on acute lung injury induced by LPS in mice
1 Departamento de Patologia (LIM05) da Faculdade de Medicina da Universidade de São Paulo, Av. Dr. Arnaldo, 455 sala 1155, CEP 01246-903, São Paulo, Brazil
2 Departamento de Clínica Médica (LIM20) da Faculdade de Medicina da Universidade de São Paulo, Av. Dr. Arnaldo, 455 sala 1226, CEP 01246-903, São Paulo, Brazil
3 Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fiocruz, Av. Brasil, 4365, CEP 21045-900, Rio de Janeiro, Brazil
4 Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Av. Prof. Lineu Prestes, 580 Bl 13B, CEP 05503-900, São Paulo, Brazil
5 Universidade Nove de Julho - UNINOVE, Rua Vergueiro 239/245, Vergueiro, CEP 01504-000, São Paulo - SP, Brazil
Critical Care 2012, 16:R199 doi:10.1186/cc11807Published: 18 October 2012
The regular practice of physical exercise has been associated with beneficial effects on various pulmonary conditions. We investigated the mechanisms involved in the protective effect of exercise in a model of lipopolysaccharide (LPS)-induced acute lung injury (ALI).
Mice were divided into four groups: Control (CTR), Exercise (Exe), LPS, and Exercise + LPS (Exe + LPS). Exercised mice were trained using low intensity daily exercise for five weeks. LPS and Exe + LPS mice received 200 µg of LPS intratracheally 48 hours after the last physical test. We measured exhaled nitric oxide (eNO); respiratory mechanics; neutrophil density in lung tissue; protein leakage; bronchoalveolar lavage fluid (BALF) cell counts; cytokine levels in BALF, plasma and lung tissue; antioxidant activity in lung tissue; and tissue expression of glucocorticoid receptors (Gre).
LPS instillation resulted in increased eNO, neutrophils in BALF and tissue, pulmonary resistance and elastance, protein leakage, TNF-alpha in lung tissue, plasma levels of IL-6 and IL-10, and IL-1beta, IL-6 and KC levels in BALF compared to CTR (P ≤0.02). Aerobic exercise resulted in decreases in eNO levels, neutrophil density and TNF-alpha expression in lung tissue, pulmonary resistance and elastance, and increased the levels of IL-6, IL-10, superoxide dismutase (SOD-2) and Gre in lung tissue and IL-1beta in BALF compared to the LPS group (P ≤0.04).
Aerobic exercise plays important roles in protecting the lungs from the inflammatory effects of LPS-induced ALI. The effects of exercise are mainly mediated by the expression of anti-inflammatory cytokines and antioxidants, suggesting that exercise can modulate the inflammatory-anti-inflammatory and the oxidative-antioxidative balance in the early phase of ALI.