Exposure to diesel exhaust particles (DEP) results in lung inflammation. Regular aerobic exercise improves the inflammatory status in different pulmonary diseases. However, the effects of long-term aerobic exercise on the pulmonary response to DEP have not been investigated. The present study evaluated the effect of aerobic conditioning on the pulmonary inflammatory and oxidative responses of mice exposed to DEP.
BALB/c mice were subjected to aerobic exercise five times per week for 5 wk, concomitantly with exposure to DEP (3 mg·mL−1; 10 μL per mouse). The levels of exhaled nitric oxide, reactive oxygen species, cellularity, interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) were analyzed in bronchoalveolar lavage fluid, and the density of neutrophils and the volume proportion of collagen fibers were measured in the lung parenchyma. The cellular density of leukocytes expressing IL-1β, keratinocyte chemoattractant (KC), and TNF-α in lung parenchyma was evaluated with immunohistochemistry. The levels of IL-1β, KC, and TNF-α were also evaluated in the serum.
Aerobic exercise inhibited the DEP-induced increase in the levels of reactive oxygen species (P < 0.05); exhaled nitric oxide (P < 0.01); total (P < 0.01) and differential cells (P < 0.01); IL-6 and TNF-α levels in bronchoalveolar lavage fluid (P < 0.05); the level of neutrophils (P < 0.001); collagen density in the lung parenchyma (P < 0.05); the levels of IL-6, KC, and TNF-α in plasma (P < 0.05); and the expression of IL-1β, KC, and TNF-α by leukocytes in the lung parenchyma (P < 0.01).
We conclude that long-term aerobic exercise presents protective effects in a mouse model of DEP-induced lung inflammation. Our results indicate a need for human studies that evaluate the pulmonary responses to aerobic exercise chronically performed in polluted areas.
1Laboratory of Experimental Air Pollution (LIM 05), Department of Pathology, University of São Paulo, School of Medicine, São Paulo, BRAZIL; 2Post Graduate Program in Biophotonics Applied to Health Sciences, Nove de Julho University, São Paulo, BRAZIL; 3Laboratory of Experimental Therapeutics (LIM 20), Department of Clinical Medicine, School of Medicine, University of São Paulo, São Paulo, BRAZIL; 4Laboratory of Cellular Biology (LIM 59), Department of Pathology, School of Medicine, University of São Paulo, São Paulo, BRAZIL; and 5Laboratory of Immunopharmacology, Oswaldo Cruz Foundation, Institute Oswaldo Cruz, Rio de Janeiro, BRAZIL
Address for correspondence: Rodolfo de Paula Vieira, M.Sc., Ph.D., University of Sao Paulo, Avenida Doutor Arnaldo 455, 01246-903, São Paulo, Brazil; E-mail: email@example.com.
Submitted for publication July 2011.
Accepted for publication December 2011.