Aerobic Exercise Attenuates Kidney Injury, Improves Physical Performance, and Increases Antioxidant Defenses in Lungs of Adenine-Induced Chronic Kidney Disease Mice.

The association between chronic kidney disease (CKD) and pulmonary pathophysiological changes is well stablished. Nevertheless, the effects of aerobic exercise (AE) on lungs of CKD need further clarification. Thus, Swiss mice were divided in control, AE, CKD, and CKD + AE groups. CKD was induced by 0.2% adenine intake during 8 weeks (4 weeks of CKD induction and 4 weeks of AE). AE consisted in running on treadmill, at moderate intensity, 30 min/day, 5 days/week, during 4 weeks. Twenty-four hours after the last training day, functional capacity test was performed, and 48 h after the test, mice were euthanized. CKD mice showed a significant increase in urine output, serum urea, and creatinine concentrations, and decreased body weight and urine density, besides oxidative damage (p = 0.044), edema area (p < 0.001), leukocyte infiltration (p = 0.040), and collagen area in lung tissue (p = 0.004). AE resulted in an increase of distance traveled (p = 0.049) and maximum speed (p = 0.046), increased activity of catalase (p = 0.031) and glutathione peroxidase (p = 0.048) in lungs, increased levels of nitric oxide (NOx) in serum (p = 0.001) and bronchoalveolar lavage fluid (p = 0.047), and decreased kidney histological injury (p = 0.018) of CKD mice. However, AE also increased oxidative damage (p = 0.003) and did not change collagen content or perivascular edema in lungs (p > 0.05) of CKD mice. Therefore, AE attenuated kidney injury and improved antioxidants defenses in lungs. Despite no significant changes in pulmonary damage, AE significantly improved physical performance in CKD mice.

Exercise Improves Lung Inflammation, but Not Lung Remodeling and Mechanics in a Model of Bleomycin-Induced Lung Fibrosis.

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-ß 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-ß. 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.

Effects of physical exercise on lung inflammation in animal models of chronic allergic lung inflammation: a systematic review.

We performed a systematic review to identify and summarize the effects of distinctive aerobic exercise (AE) protocols on chronic allergic lung inflammation reported in asthma animal models. We identified 255 preclinical studies of asthma and AE protocols by comprehensive searches in PubMed, ScienceDirect and LILACS for peer-reviewed journals, using the search components "exercise," "lung inflammation," and "asthma," without restrictions on publication date. Twenty-two studies were selected that met all eligibility criteria. Most studies used an ovalbumin experimental model and performed experiments with BALB/c mice. Most studies performed treadmill AE, using protocols of 30 to 60 minutes, 3 to 5 times/week, for 4 to 8 weeks. The results showed that the effects of AE on lungs were protocol dependent, but generaly, there was a decrease in inflammatory cell influx and Th2 cytokines, as well as an increase in anti-inflammatory defenses. However, the immunoregulation of globulins and nitric oxide levels in asthma seemed to be associated with the onset of AE. The results suggest that AE plays an important immunoregulatory role in animal models of asthma, with effects mainly mediated by increased anti-inflammatory defenses and reduced Th2 response. In parallel, prophylactic and therapeutic AE also played important roles in decreasing bronchial responsiveness and attenuating lung remodeling in animal models of asthma, secondary outcomes in this systematic review. The review protocol was published for free access in October 2017 on the Systematic Review Facility (SyRF) platform (http://syrf.org.uk/protocols/).

Pulmonary and muscle profile in pneumosepsis: A temporal analysis of inflammatory markers.

In sepsis, greater understanding of the inflammatory mechanism involved would provide insights into the condition and into its extension to the muscular apparatus in critically ill patients. Therefore, this study evaluates the inflammatory profile of pneumosepsis induced by Klebsiella pneumoniae (K.p.) in lungs and skeletal muscles during the first 72 h. Male BALB/c mice were divided into 4 groups, submitted to intratracheal inoculation of K.p. at a concentration of 2 × 108 (PS) or PBS, and assessed after 24 (PS24), 48 (PS48) and 72 (PS72) hours. The Maximum Physical Capacity Test (MPCT) was performed before and after induction. Pulmonary inflammation was assessed by total cell number, nitric oxide levels (NOx), IL-1ß and TNF-α levels in bronchoalveolar lavage fluid (BALF); inflammation and muscle trophism were evaluated by the levels of TNF-α, IL-6, TGF-ß and BDNF by ELISA and NF-κB by western blotting in muscle tissue. Cells and colony forming units (CFU) were also analyzed in blood samples. The PS groups showed an increase in total cells in the BALF (p < 0.05), as well in the number of granulocytes in the blood (p < 0.05) and a decrease in performance in the MPCT (p < 0.05). NOx levels showed significant increase in PS72, when compared to Control group (p = 0.03). The PS24 showed a significant increase lung in TNF-α levels (p < 0.001) and in CFU (p = 0.013). We observed an increase in muscular IL-6 and nuclear NF-κB levels in PS24 group, when compared to PS48 and Control groups (p < 0.05). Nevertheless, mild signs of injury in the skeletal muscle tissue does not support the idea of an early muscular injury in this experimental model, suggesting that the low performance of the animals during the MPCT may be related to lung inflammation.