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AE attenuated dendritic cell and lymphocyte activation and maturation, which contributed to reduced airway inflammation and remodeling in the OVA model of chronic allergic airway inflammation.

IntroductionThe aim of this study was to investigate the effect of aerobic exercise (AE) in reducing bleomycin-induced fibrosis in mice of a Th2-dominant immune background (BALB/c).MethodsBALB/c mice were distributed into: sedentary, control (CON), Exercise-only (EX), sedentary, bleomycin-treated (BLEO) and bleomycin-treated+exercised (BLEO+EX); (n = 8/group). Following treadmill adaptation, 15 days following a single, oro-tracheal administration of bleomycin (1.5U/kg), AE was performed 5 days/week, 60min/day for 4 weeks at moderate intensity (60% of maximum velocity reached during a physical test) and assessed for pulmonary inflammation and remodeling, and cytokine levels in bronchoalveolar lavage (BAL).ResultsAt 45 days post injury, compared to BLEO, BLEO+EX demonstrated reduced collagen deposition in the airways (p<0.001) and also in the lung parenchyma (p<0.001). In BAL, a decreased number of total leukocytes (p<0.01), eosinophils (p<0.001), lymphocytes (p<0.01), macrophages (p<0.01), and neutrophils (p<0.01), as well as reduced pro-inflammatory cytokines (CXCL-1; p<0.01), (IL-1β; p<0.001), (IL-5; p<0.01), (IL-6; p<0.001), (IL-13; p<0.01) and pro-fibrotic growth factor IGF-1 (p<0.001) were observed. Anti-inflammatory cytokine IL-10 was increased (p<0.001).ConclusionAE attenuated bleomycin-induced collagen deposition, inflammation and cytokines accumulation in the lungs of mice with a predominately Th2-background suggesting that therapeutic AE (15–44 days post injury) attenuates the pro-inflammatory, Th2 immune response and fibrosis in the bleomycin model.

Background Alterations of the circadian rhythm negatively impact several aspects of the health, including the lung function. Chronic shiftwork scale classically induces alterations in the circadian rhythm. However, its effects on pulmonary immune response are unknown. Aims To evaluate the impact of chronic alteration of circadian rhythm on pulmonary function and immune response. Methods In this context, a 12 × 24 hours and 12 × 48 hours work scale in shiftwork scale policemen (n = 25; 38.73 ± 6.92 years old) were compared with fixed work scale (8 h/d) civil men (n = 25; 34.00 ± 9.60 years old) who were evaluated for perceived stress, sleepiness, physical activity levels, anthropometric characteristics, lung function, pulmonary and systemic cellular and humoral immune response. Results Policemen presented increased levels of perceived stress (P < .0008), impaired sleepiness (P < .04) and lung function as demonstrated by reduced forced vital capacity (FVC) (P < .053) and FEV1 (P < .043) when compared with civil men. In addition, increased levels of exhaled nitric oxide (P < .037) and of IL‐2 (P < .0046) in the breath condensate revealed that policemen presented chronic lung inflammation compared with civil men. Although the whole blood analysis did not showed any differences between the two groups concerning the number of leucocytes, the humoral response revealed that policemen presented increased levels of IL‐2 (P < .002) and lower levels of IL‐10 (P < .001), clearly displaying a clinical status of low‐grade inflammation. Conclusions Chronic alteration of circadian rhythm in shiftwork scale policemen results in impaired lung function, beyond to impair pulmonary and systemic immune function.

Air pollution is a growing problem worldwide, inducing and exacerbating several diseases. Among the several components of air pollutants, particulate matter (PM), especially thick (10-2.5 µm; PM 10) and thin (≤2.5 µm; PM 2.5), are breathable particles that easily can be deposited within the lungs, resulting in pulmonary and systemic inflammation. Although physical activity is strongly recommended, its effects when practiced in polluted environments are questionable. Therefore, the present study evaluated the pulmonary and systemic response of concomitant treadmill training with PM 2.5 and PM 10 exposure. Treadmill training inhibited PM 2.5- and PM 10-induced accumulation of total leukocytes (p<0.001), neutrophils (p<0.001), macrophages (p<0.001) and lymphocytes (p<0.001) in bronchoalveolar lavage (BAL), as well as the BAL levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.05). Similar effects were observed on accumulation of polymorphonuclear (p<0.01) and mononuclear (p<0.01) cells in the lung parenchyma and in the peribronchial space. Treadmill training also inhibited PM 2.5- and PM 10-induced systemic inflammation, as observed in the number of total leukocytes (p<0.001) and in the plasma levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.001). Treadmill training inhibits lung and systemic inflammation induced by particulate matter.

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Purpose Evaluate the participation of STAT3 in the effects of aerobic exercise (AE) in a model of smoke-induced COPD. Methods C57Bl/6 male mice were divided into control, Exe, COPD, and COPD+Exe groups. Smoke were administered during 90 days. Treadmill aerobic training begun on day 61 until day 90. Pulmonary inflammation, systemic inflammation, the level of lung emphysema, and the airway remodeling were evaluated. Analysis of integral and phosphorylated expression of STAT3 by airway epithelial cells, peribronchial leukocytes, and parenchymal leukocytes was performed. Results AE inhibited smoke-induced accumulation of total cells (p < 0.001), lymphocytes (p < 0.001), and neutrophils (p < 0.001) in BAL, as well as BAL levels of IL-1β (p < 0.001), CXCL1 (p < 0.001), IL-17 (p < 0.001), and TNF-α (p < 0.05), while increased the levels of IL-10 (p < 0.001). AE also inhibited smoke-induced increases in total leukocytes (p < 0.001), neutrophils (p < 0.05), lymphocytes (p < 0.001), and monocytes (p < 0.01) in blood, as well as serum levels of IL-1β (p < 0.01), CXCL1 (p < 0.01), IL-17 (p < 0.05), and TNF-α (p < 0.01), while increased the levels of IL-10 (p < 0.001). AE reduced smoke-induced emphysema (p < 0.001) and collagen fiber accumulation in the airways (p < 0.001). AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells (p < 0.001), peribronchial leukocytes (p < 0.001), and parenchymal leukocytes (p < 0.001). Conclusions AE reduces smoke-induced COPD phenotype involving STAT3.

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.