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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-β 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-β. 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.

The low-grade inflammation associated with metabolic syndrome (MS) triggers functional and structural alterations in several organs. Whereas lung function impairment is well reported for older adult population, the effect of MS on functional and immunological responses in the lungs remains unclear. In this cross-sectional study we determined whether MS alters pulmonary function, and immunological responses in older adults with MS. The study sample consisted of older adults with MS (68 ± 3 years old; n = 77) and without MS (67 ± 3 years old; n = 77). Impulse oscillometry was used to evaluate airway and tissue resistance, and reactance. Biomarkers of inflammation and fibrosis were assessed in the blood and in breath condensate. The total resistance of the respiratory system (R5Hz; p < 0.009), and the resistance of the proximal (R20Hz; p < 0.001) and distal (R5Hz–R20Hz; p < 0.004) airways were higher in MS individuals compared to those without MS. Pro-inflammatory (leptin, IL-1beta, IL-8, p < 0.001; TNF-alpha, p < 0.04) and anti-inflammatory cytokines (adiponectin, IL-1ra, IL-10, p < 0.001), anti-fibrotic (relaxin 1, relaxin 3, Klotho, p < 0.001) and pro-fibrotic (VEGF, p < 0.001) factors were increased in sera and in breath condensate individuals with MS. The results show that MS adversely affect lung mechanics, function, and immunological response in older adults. The data offer a metabolic basis for the inflammaging of the lungs and suggest the lungs as a potential therapeutic target for controlling the immune response and delaying the onset of impaired lung function in older adults with MS.

Objective The Parkinson Anxiety Scale (PAS) was developed to measure the severity of anxiety symptoms in patients with Parkinson’s disease (PD), and it has not yet been adapted and validated in Portuguese. Thus, this study evaluated the reliability and validity of a translated and adapted version of the PAS for the Brazilian population of PD patients. Methods The Parkinson Anxiety Scale – Brazilian Version (PAS-BV) was completed by 55 patients with PD. The reliability (test-retest reliability, interrater reliability and internal consistency) and construct validity of the PAS-BV were assessed by comparing it with the Beck Anxiety Inventory (BAI), the Parkinson’s Disease Fatigue Scale (PFS) and the Unified Parkinson Disease Rating Scale (UPDRS) part III. Results Patients with PD had an average age of 64.51 ± 9.20 years and had PD for an average of 6.98 ± 5.02 years. The reliability of the PAS-BV was 0.83, and the intraclass correlation coefficient (ICC) (retest-test) was 0.88. The scale presented good convergent validity with the BAI ( r s = 0.82, p < 0.05). It also presented good divergent validity with the PFS ( r s = 0.24, p > 0.05) and the UPDRS part II ( r s = -0.10, p > 0.05), part III ( r s = -0.21, p > 0.05), and part IV ( r s = 0.03, p > 0.05), as indicated by the absence of significant correlations. However, there was a significant correlation between the PAS-BV and part I of the UPDRS ( r s = 0.67, p < 0.05). Conclusion The PAS-BV presents substantial reliability and validity for patients with PD without dementia.

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Background: Asthmatic children present variable degrees of airway inflammation, remodeling and resistance, which correlates with disease control and severity. Chronic inflammatory process of the airways triggers airway remodeling, which reflects the degree of airway resistance. Pro-inflammatory and pro-fibrotic mediators are centrally involved in this process. This study has investigated for the first time, whether the levels of pulmonary and systemic pro-inflammatory and pro-fibrotic mediators present correlation with the resistance of respiratory system and of proximal and distal airways. Methods: 24 asthmatic children (persistent mild and moderate) and 24 non-asthmatic children (both between 6-13 years old) were evaluated for anthropometric characteristics, lung function and mechanics, pulmonary and systemic immune response. Results: Asthmatic children showed an increased number of blood eosinophils (p<0.04), basophils (p<0.04), monocytes (p<0.002) and lymphocytes (p<0.03). In addition, asthmatic children showed an impaired lung function, as demonstrated by FEV1%pred. (p<0.0005) and FEV1/FVC (p<0.004), decreased total resistance of respiratory system (R5Hz; p<0.009), increased resistance of proximal airways (R20Hz; p<0.02), increased elastance (Z5Hz; p<0.02) and increased reactance (X5Hz; p<0.002). Moreover, the following inflammatory factors were significantly higher in asthmatic than non-asthmatic children: GM-CSF in the breath condensate (BC) (p<0.0001) and in the serum (p<0.0001); TGF-beta in the BC (p<0.0001) and in the serum (p<0.004); IL-5 in the BC (p<0.02) and in the serum (p<0.01); IL-4 in the serum (p<0.0002). Conclusions: Impulse oscillometry is a sensitive method to detect airway resistance in asthmatic children, reflecting airway remodeling, an event followed by increased levels of pro-inflammatory and pro-fibrotic mediators.

Low-grade inflammation associated with metabolic syndrome (MS) triggers alterations in several organs, but its effects on pulmonary functional and immunological response in older adults are unknown. This cross-sectional study investigated such responses in older adults with and without MS. The study consisted of 77 older adults with MS (68 ± 3 years old) and without MS (67 ± 3 years old). Impulse oscillometry (IOS) was used to evaluate airway and tissue resistance and reactance. Biomarkers of systemic and pulmonary inflammation and fibrosis were studied. Total resistance of respiratory system (R5Hz; p < 0.009), and resistance of proximal (R20Hz; p < 0.001) and distal (R5Hz-R20Hz; p < 0.004) airways were impaired in MS individuals compared to those without MS. The levels of pro-inflammatory (leptin; IL-1beta; IL-8, p < 0.001; TNF-alpha, p < 0.04) and pro-fibrotic (VEGF, p < 0.001) factor increased in MS, while reduced levels of anti-inflammatory cytokines (adiponectin; IL-1ra; IL-10; p < 0.001), and anti-fibrotic (relaxin 1; relaxin 3; Klotho, p < 0.001) factors were found. We conclude that MS accelerates lung function and mechanics impairment in older adults in detriment of an imbalance between pro and anti-inflammatory and fibrotic mediators. Furthermore, this study shows that the lungs also are a target organ in MS, deserving clinical assessment in older adults’ population.

Background: Obesity impairs lung function and mechanics and leads to low-grade inflammation, but the effects of combined physical exercise (CPE) on that are unknown.Methods: We investigated the effects of 12 weeks of combined physical exercise (aerobic + resistance training), in non-obese (n = 12), overweight (n = 17), and obese grade I (n = 11) women. Lung function and lung mechanics were evaluated. The systemic immune response was evaluated by whole blood analysis and biomarker measurements, while pulmonary fibrotic biomarkers were evaluated in the breath condensate.Result: CPE improved forced vital capacity (FVC) % (p &lt; 0.001) and peak expiratory flow (PEF) % (p &lt; 0.0003) in the obese group; resistance of the respiratory system (R5Hz) in non-obese (p &lt; 0.0099), overweight (p &lt; 0.0005), and obese (p &lt; 0.0001) groups; resistance of proximal airways (R20Hz) in non-obese (p &lt; 0.01), overweight (p &lt; 0.0009), and obese (p &lt; 0.0001) groups; resistance of distal airways (R5Hz–R20Hz) in non-obese (p &lt; 0.01), overweight (p &lt; 0.0012), and obese (p &lt; 0.0001) groups; reactance of the respiratory system (X5Hz) in non-obese (p &lt; 0.01), overweight (p &lt; 0.0006), and obese (p &lt; 0.0005) groups; impedance of the respiratory system (Z5Hz) in non-obese (p &lt; 0.0099), overweight (p &lt; 0.0005), and obese (p &lt; 0.0001) groups; central resistance (RCentral) in non-obese (p &lt; 0.01), overweight (p &lt; 0.001), and obese (p &lt; 0.0003) groups; and the peripheral resistance (RPeripheral) in non-obese (p &lt; 0.03), overweight (p &lt; 0.001), and obese (p &lt; 0.0002) groups. CPE reduced the pro-fibrotic IGF-1 levels in BC in overweight (p &lt; 0.0094) and obese groups (p &lt; 0.0001) and increased anti-fibrotic Klotho levels in BC in obese (p &lt; 0.0001) groups, and reduced levels of exhaled nitric oxide in overweight (p &lt; 0.03) and obese (p &lt; 0.0001) groups.Conclusion: CPE improves lung function, mechanics, and pulmonary immune response in overweight and obese grade I women by increasing anti-fibrotic protein Klotho and reducing pro-fibrotic IGF-1.