Several benefits of aerobic training for asthmatic patients have been demonstrated. However, its effects on systemic inflammation and on airway remodeling mediators and lung mechanics are unknown. This prospective study included 21 intermittent and mild asthma patients, and as primary outcomes, the evaluation of pro- and anti-inflammatory and pro- and antifibrotic mediators in exhaled breath condensate (EBC) and blood were performed, beyond the cell counting in blood and in induced sputum. Aerobic training was performed for 3 months, 3 times per week. Aerobic training increased the levels of anti-inflammatory cytokines and of antifibrotic mediators in the breath condensate: IL-1ra ( p = 0.0488 ), IL-10 ( p = 0.0048 ), relaxin-3 ( p = 0.0019 ), and klotho ( p < 0.0043 ), respectively. Similarly, in plasma, increased levels of IL-1ra ( p = 0.0147 ), IL-10 ( p < 0.0001 ), relaxin-3 ( p = 0.004 ), and klotho ( p = 0.0023 ) were found. On contrary, reduced levels of proinflammatory cytokines in the breath condensate, IL-1β ( p = 0.0008 ), IL-4 ( p = 0.0481 ), IL-5 ( p < 0.0001 ), IL-6 ( p = 0.0032 ), IL-13 ( p = 0.0013 ), and TNF-α ( p = 0.0001 ) and profibrotic markers VEGF ( p = 0.0017 ) and TSLP ( p = 0.0056 ) were found. Similarly, in plasma, aerobic training significantly reduced the levels of proinflammatory cytokines IL-1β ( p = 0.0008 ), IL-4 ( p = 0.0104 ), IL-5 ( p = 0.0001 ), IL-6 ( p = 0.006 ), IL-13 ( p = 0.0341 ), and TNF-α ( p = 0.0003 ) and of profibrotic markers VEGF ( p = 0.0009 ) and TSLP ( p < 0.0076 ). Fractional exhaled nitric oxide (FeNO) was reduced after the intervention ( p = 0.0313 ). Regarding inflammatory cells in sputum, there was a reduction in total cells ( p = 0.008 ), eosinophils ( p = 0.009 ), and macrophages ( p = 0.020 ), as well as of blood eosinophils ( p = 0.0203 ) and lymphocytes ( p = 0.0198 ). Aerobic training positively modulates chronic airway inflammation and remodeling mediators, beyond to improve systemic inflammation in intermittent and mild asthmatic patients.
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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