Collagen-based products are found in different pharmaceuticals, medicine, food, and cosmetics products for a wide variety of applications. However, its use to prevent or improve the health of skin is growing dizzyingly. Therefore, this study investigated whether collagen peptides could induce fibroblast and keratinocyte proliferation and activation beyond reducing an inflammatory response induced by lipopolysaccharide (LPS). Human skin fibroblasts (CCD-1072Sk) and human keratinocytes (hKT-nh-skp-KT0026) were seeded at a concentration of 5 × 10⁴ cells/mL. LPS (10 ng/mL) and three doses of collagen peptides (2.5 mg/mL, 5 mg/mL, 10 mg/mL) were used. The readout parameters were cell proliferation; expression of inducible nitric oxide synthase (iNOS); expression of pro-collagen-1α by fibroblasts; and secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) by both cell types. The results demonstrated that all doses of collagen supplementation induced increased proliferation of both human fibroblasts (p < 0.01) and human keratinocytes (p < 0.001), while only the dose of 10 mg/mL induced an increased expression of pro-collagen-1α by fibroblasts. Similarly, only the dose of 10 mg/mL reduced LPS-induced iNOS expression in fibroblasts (p < 0.05) and keratinocytes (p < 0.01). In addition, collagen supplementation reduced the LPS-induced IL-1β (p < 0.05), IL-6 (p < 0.001), IL-8 (p < 0.01), and TNF-α (p < 0.05), and increased the TGF-β and VEGF expression in fibroblasts. Furthermore, collagen supplementation reduced the LPS-induced IL-1β (p < 0.01), IL-6 (p < 0.01), IL-8 (p < 0.01), and TNF-α (p < 0.001), and increased the TGF-β (p < 0.05) and VEGF (p < 0.05) expression in keratinocytes. In conclusion, collagen peptides were found to induce fibroblast and keratinocyte proliferation and pro-collagen-1α expression, involving increased expression of TGF-β and VEGF, as well as the suppression of an inflammatory response induced by LPS.

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.

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.

Introduction: We sought to evaluate the effects of a 12-week pulmonary rehabilitation (PR) program on lung function, mechanics, as well as pulmonary and systemic inflammation in a cohort of 33 individuals with moderate to severe post-COVID-19. Material and Methods: The pulmonary rehabilitation (PR) program employed a combination of aerobic and resistance exercises. Thirty minutes of treadmill training at 75% of the maximum heart rate, combined with 30 min resistance training consisting of 75% of one maximum repetition, three times a week throughout 12 weeks. Results: PR improved the lung function, FVC (p < 0.02), FEV1 (p < 0.02), FEV1/FVC (p < 0.01), MEF25% (p < 0.006), MEF50% (p < 0.03), and MEF75% (p < 0.02). PR also positively influenced lung mechanics, reducing respiratory impedance (Z5Hz, p < 0.03), respiratory reactance (X5Hz, p < 0.01), resistance of the entire respiratory system (R5Hz, p < 0.03), central airway resistance (RCentral, p < 0.03), and peripheral airway resistance (RPeripheral, p < 0.02). Moreover, muscle strength gains were evident, with significant improvements observed in hand grip strength for both the right (p < 0.02) and left (p < 0.01) hands, as well as maximal inspiratory (p < 0.02) and expiratory (p < 0.03) pressures. Additionally, PR exhibited anti-inflammatory effects by reducing the pro-inflammatory cytokines IL-1β (p < 0.0001) and IL-6 (p < 0.0001) and increasing the anti-inflammatory IL-1RA (p < 0.0004) and IL-10 (p < 0.003) and anti-viral IFN-γ (p < 0.0002) and IFN-β (p < 0.008) cytokines in breath condensate and serum samples. Conclusions: Collectively, these findings highlight the effectiveness of PR in ameliorating COVID-19 sequel across respiratory system, skeletal muscle, and immune responses. This highlights its promising potential as a therapeutic intervention for individuals recovering from COVID-19.

The 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). BALB/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). At 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). AE 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.

Aim: Physical activity attenuates hypertension in older adults, but its impact on pulmonary function and mechanics in hypertensive older adults is unknown. The study seeks to understand whether a physically active lifestyle can improve respiratory capacity, the mechanical efficiency of the lungs, and, consequently, the quality of life of these individuals, comparing data between groups of active and sedentary hypertensive older adults. Methods: This is a cross-sectional study. We evaluated 731 older adults, stratified into two initial groups: hypertensive older adults (HE; n = 445) and non-hypertensive older adults (NHE; n = 286). For a secondary analysis, we used the International Physical Activity Questionnaire to sub-stratify HE and NHE into four groups: physically inactive hypertensive (PIH; n = 182), active hypertensive (AH; n = 110), physically inactive non-hypertensive (PINH; n = 104), and active non-hypertensive (ANH; n = 65). Lung function was measured by spirometry, and lung mechanics were assessed by impulse oscillometry. Results: Hypertensive older adults presented reduced lung function compared to non-hypertensive older adults, and physical inactivity accentuated this decline. Regarding pulmonary mechanics, hypertensive older adults had higher resistance of the entire respiratory system (R5 Hz), the central airways (R20 Hz), and peripheral airways (R5–20 Hz), which may trigger bronchoconstriction. Conclusions: Hypertension is associated with impaired lung function and mechanics in older adults, and a physically active lifestyle attenuates these dysfunctions.