RESUMO
INTRODUCTION/PURPOSE: Obesity increases significantly every year worldwide. Since 1980, the prevalence of individuals with obesity has practically doubled. Obesity plays an important role in the pathophysiology of diseases that arise from a complex interaction of nutritional, genetic, and metabolic factors, characterizing a chronic inflammatory state. This study aimed to verify the systemic inflammatory response through the analysis of IGF-1, IL-23, and resistin levels and the lipid profile in severely obese women undergoing surgery for obesity and weight-related diseases. MATERIALS AND METHODS: This randomized controlled clinical trial includes female patients clinically diagnosed with severe obesity with an indication for bariatric surgery. RESULTS: In the initial evaluation, no significant difference was observed between the control (CG) and bariatric surgery (BSG) groups. The weight, BMI, systolic and diastolic blood pressures, total cholesterol, LDL, HDL, total non-HDL cholesterol, and glucose in BSG patients showed a significant change after surgery. Pre- and post-surgery levels of resistin, IGF-1, and IL-23 showed a significant difference in the BSG group, but only IL-23 was changed after 6 months in the CG. CONCLUSION: The results of this study confirmed that weight loss induced by surgery for obesity and weight-related diseases improved the lipid profile and reduced the chronic inflammatory status in women with severe obesity.
Assuntos
Cirurgia Bariátrica , Obesidade Mórbida , Cirurgia Bariátrica/métodos , Feminino , Humanos , Inflamação , Obesidade/complicações , Obesidade/cirurgia , Obesidade Mórbida/cirurgia , Redução de Peso/fisiologiaRESUMO
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.
Assuntos
Pulmão/fisiopatologia , Síndrome Metabólica/fisiopatologia , Testes de Função Respiratória , Idoso , Antropometria , Biomarcadores/metabolismo , Estudos Transversais , Citocinas/metabolismo , Feminino , Força da Mão , Humanos , Inflamação , Masculino , Pessoa de Meia-Idade , Força Muscular , Oscilometria , Fibrose Pulmonar/fisiopatologia , Fenômenos Fisiológicos RespiratóriosRESUMO
OBJECTIVES: To compare the inflammatory and oxidative stress (OS) states of adults with bronchiectasis with those of healthy controls and correlate inflammatory and OS levels with lung function and physical capacity. METHODS: This study used a cross-sectional design. Seventy-four adults with bronchiectasis (age: 49±15 years, forced expiratory volume in 1 second [FEV1]: 52.5±25.6%) and 42 healthy controls (age: 44±17 years, FEV1: 95.9±14.0%) performed cardiopulmonary exercise tests and incremental shuttle walking tests. Their physical activity in daily life, inflammatory cytokine, and antioxidant levels in plasma were measured. RESULTS: Compared to that of the controls, the levels of interleukin (IL)-6 (p<0.001), IL-10 (p<0.001), carbonylated proteins (p=0.001), and superoxide anions (p=0.046) were significantly increased in adults with bronchiectasis. Catalase activity was also reduced in this group (p<0.001). The inflammatory markers IL-1ß, IL-6, and tumor necrosis factor-α correlated negatively with aerobic capacity (r=-0.408, r=-0.308, and r=-0.207, respectively). We observed similar correlations with OS markers (thiobarbituric acid and carbonyls; r=-0.290 and r=0.379, respectively), and these markers also significantly correlated with the aerobic capacity. CONCLUSIONS: Adults with bronchiectasis presented an increased systemic inflammatory response that correlated negatively with physical capacity.
Assuntos
Bronquiectasia , Adulto , Estudos Transversais , Tolerância ao Exercício , Humanos , Inflamação , Pessoa de Meia-Idade , Estresse OxidativoRESUMO
OBJECTIVES: To compare the inflammatory and oxidative stress (OS) states of adults with bronchiectasis with those of healthy controls and correlate inflammatory and OS levels with lung function and physical capacity. METHODS: This study used a cross-sectional design. Seventy-four adults with bronchiectasis (age: 49±15 years, forced expiratory volume in 1 second [FEV1]: 52.5±25.6%) and 42 healthy controls (age: 44±17 years, FEV1: 95.9±14.0%) performed cardiopulmonary exercise tests and incremental shuttle walking tests. Their physical activity in daily life, inflammatory cytokine, and antioxidant levels in plasma were measured. RESULTS: Compared to that of the controls, the levels of interleukin (IL)-6 (p<0.001), IL-10 (p<0.001), carbonylated proteins (p=0.001), and superoxide anions (p=0.046) were significantly increased in adults with bronchiectasis. Catalase activity was also reduced in this group (p<0.001). The inflammatory markers IL-1β, IL-6, and tumor necrosis factor-α correlated negatively with aerobic capacity (r=-0.408, r=-0.308, and r=-0.207, respectively). We observed similar correlations with OS markers (thiobarbituric acid and carbonyls; r=-0.290 and r=0.379, respectively), and these markers also significantly correlated with the aerobic capacity. CONCLUSIONS: Adults with bronchiectasis presented an increased systemic inflammatory response that correlated negatively with physical capacity.
Assuntos
Humanos , Adulto , Pessoa de Meia-Idade , Bronquiectasia , Estudos Transversais , Tolerância ao Exercício , Estresse Oxidativo , InflamaçãoRESUMO
OBJECTIVES: Some pro-inflammatory lipids derived from 1 lipooxygenase enzyme are potent neutrophil chemoattractant, a cell centrally involved in acute respiratory distress syndrome (ARDS); a syndrome lacking effective treatment. Considering the beneficial effects of the leukotriene receptor inhibitor, montelukast, on other lung diseases, whether montelukast attenuates inflammation in a mouse model of ARDS, and whether it reduces LPS stimulated activation of human neutrophils was investigated. METHODS: Thirty-five C57Bl/6 mice were distributed into control (PBS)+24h, LPS+24h (10µg/mouse), control+48h, LPS+48h, and LPS 48h+Montelukast (10mg/kg). In addition, human neutrophils were incubated with LPS (1µg/mL) and treated with montelukast (10µM). RESULTS: Oral-tracheal administration of montelukast significantly attenuated total cells (P<.05), macrophages (P<.05), neutrophils (P<.01), lymphocytes (P<.001) and total protein levels in BAL (P<.05), as well as IL-6 (P<.05), CXCL1/KC (P<.05), IL-17 (P<.05) and TNF-α (P<.05). Furthermore, montelukast reduced neutrophils (P<.001), lymphocytes (P<.01) and macrophages (P<.01) in the lung parenchyma. In addition, montelukast restored BAL VEGF levels (P<.05). LTB4 receptor expression (P<.001) as well as NF-κB (P<.001), a downstream target of LPS, were also reduced in lung parenchymal leukocytes. Furthermore, montelukast reduced IL-8 (P<.001) production by LPS-treated human neutrophils. CONCLUSION: In conclusion, montelukast efficiently attenuated both LPS-induced lung inflammation in a mouse model of ARDS and in LPS challenged human neutrophils.
Assuntos
Acetatos/farmacologia , Antagonistas de Leucotrienos/farmacologia , Ativação de Neutrófilo/efeitos dos fármacos , Pneumonia/prevenção & controle , Quinolinas/farmacologia , Animais , Lavagem Broncoalveolar , Permeabilidade Capilar/efeitos dos fármacos , Ciclopropanos , Citocinas/análise , Citocinas/efeitos dos fármacos , Humanos , Contagem de Leucócitos , Lipopolissacarídeos , Pulmão/citologia , Linfócitos/efeitos dos fármacos , Macrófagos/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos C57BL , NF-kappa B/efeitos dos fármacos , NF-kappa B/metabolismo , Neutrófilos/efeitos dos fármacos , Neutrófilos/metabolismo , Pneumonia/induzido quimicamente , Receptores do Leucotrieno B4/efeitos dos fármacos , Receptores do Leucotrieno B4/metabolismo , Síndrome do Desconforto Respiratório/induzido quimicamente , Síndrome do Desconforto Respiratório/etiologia , Sulfetos , Fatores de Tempo , Fator A de Crescimento do Endotélio Vascular/metabolismoRESUMO
BACKGROUND: The endurance exercise is capable of inducing skeletal muscle, heart, and respiratory fatigue, evidenced by morphofunctional cardiac changes, release of myocardial injury biomarkers, and reduction of maximal voluntary ventilation and oxygen consumption (VO2) at peak exercise. PURPOSE: The aim of this study was to investigate whether marathoners present cardiac fatigue after marathon and whether it correlates with pulmonary levels of exhaled nitric oxide (eNO) and pulmonary inflammation. METHODS: 31 male marathoners, age 39 ± 9 years, were evaluated by cardiopulmonary exercise test three weeks before and between three and 15 days after a marathon; eNO analysis and spirometry were evaluated before, immediately after, and 24 and 72 hours after the marathon, and sputum cellularity and cytokine level were assessed before and after the marathon. RESULTS: Marathon induced an increase in the percentage of macrophages, neutrophils (from 0.65% to 4.28% and 6.79% to 14.11%, respectively), and epithelial cells and a decrease in cytokines in induced sputum, followed by an increase in eNO concentration (20 ± 11 to 35 ± 19 ppb), which presented a significant reduction 24 and 72 hours after marathon (9 ± 12 e 12 ± 9 ppb, p < 0.05). We observed a decrease in the spirometry parameters in all time points assessed after the marathon (p < 0.05) as well as in cardiopulmonary capacity, evidenced by a reduction in VO2 and ventilation peaks (57 ± 6 to 55 ± 6 mL·min-1·Kg-1 and 134 ± 19 to 132 ± 18 Lpm, respectively, p < 0.05). Finally, we observed a negative correlation between the decrease in forced expiratory volume and decrease in eNO 24 and 72 hours after marathon (r = -0.4, p = 0.05). CONCLUSION: Reduction in eNO bioavailability after marathon prevents the reduction in cardiopulmonary capacity induced by acute inflammatory pattern after marathon.
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Teste de Esforço , Expiração , Óxido Nítrico/metabolismo , Corrida/fisiologia , Adulto , Citocinas/metabolismo , Humanos , Inflamação/patologia , Pulmão/patologia , Masculino , Escarro/metabolismoRESUMO
Creatine (Cr) is a substrate for adenosine triphosphate synthesis, and it is the most used dietary supplement among professional and recreative athletes and sportsmen. Creatine supplementation may increase allergic airway response, but the cellular and molecular mechanisms are unknown. We used murine model of OVA-induced chronic asthma and showed that Cr supplementation increased total proteins, ATP level, lymphocytes, macrophages, and IL-5 levels in BALF, as well as IL-5 in the supernatant of re-stimulated mediastinal lymph nodes. IL-5 and IL-13 expression by epithelial cells and by peribronchial leukocytes were increased by Cr. Cr augmented the expression of P2 × 7 receptor by peribronchial leukocytes and by epithelial cells, and increased the accumulation of eosinophils in peribronchial space and of collagen fibers in airway wall. In human cells, while Cr induced a release of ATP, IL-6, and IL-8 from BEAS-2B cells, whole blood cells, such as eosinophils, and CD4+ T cells, P2 × 7 receptor inhibitor (A740003) reduced such effects, as denoted by reduced levels of ATP, IL-6, and IL-8. Therefore, Cr supplementation worsened asthma pathology due to activation of airway epithelial cells and peribronchial leukocytes, involving purinergic signaling.
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Asma/patologia , Creatina/toxicidade , Suplementos Nutricionais/toxicidade , Pneumonia/patologia , Receptores Purinérgicos P2X7/metabolismo , Animais , Asma/metabolismo , Modelos Animais de Doenças , Humanos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Pneumonia/metabolismoRESUMO
The aim of this study was to evaluate the effectiveness of acute application of LEDT in improving peripheral muscle performance during isometric exercise in patients with asthma. Eleven patients, with a mean age 38 ± 10, underwent a single LEDT and sham application in the femoral quadriceps' dominant member (cluster with 50 LED λ = 850 nm, 50 mW, 15 s; 37.5 J), 48 h apart in a randomized crossover design. Before and after LEDT and sham application, the patients were submitted an isometric endurance test (60% of the maximum isometric voluntary contraction), up to the limit of tolerance simultaneous recording of surface electromyography. There were no statistically significant differences between groups at the time of contraction (before 41±14 versus 44±16; after 46±12 versus 45±20 s) during the isometric contraction test and inflammatory markers before and after a single LEDT application. A single application of LEDT in the parameters and dose according to the equipment used in the study were not able to promote differences in the time of contraction and the fatigue response in asthmatic patients. However, the chronic effects of LEDT application for improving muscle performance in these patients are unknown and may present different responses during applications for a long time.
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Asma/terapia , Exercício Físico , Contração Isométrica/fisiologia , Músculo Esquelético/fisiopatologia , Adulto , Asma/fisiopatologia , Feminino , Humanos , Terapia com Luz de Baixa Intensidade , Masculino , Pessoa de Meia-Idade , Fadiga Muscular/fisiologia , Músculo Quadríceps/fisiopatologiaRESUMO
Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by irreversible airflow limitation, airway inflammation and remodeling, and enlargement of alveolar spaces. COPD is in the top five leading causes of deaths worldwide and presents a high economic cost. However, there are some preventive measures to lower the risk of developing COPD. Low-level laser therapy (LLLT) is a new effective therapy, with very low cost and no side effects. So, our objective was to investigate if LLLT reduces pulmonary alterations in an experimental model of COPD. C57BL/6 mice were submitted to cigarette smoke for 75 days (2x/day). After 60 days to smoke exposure, the treated group was submitted to LLLT (diode laser, 660 nm, 30 mW, and 3 J/cm2) for 15 days and euthanized for morphologic and functional analysis of the lungs. Our results showed that LLLT significantly reduced the number of inflammatory cells and the proinflammatory cytokine secretion such as IL-1ß, IL-6, and TNF-α in bronchoalveolar lavage fluid (BALF). We also observed that LLLT decreased collagen deposition as well as the expression of purinergic P2X7 receptor. On the other hand, LLLT increased the IL-10 release. Thus, LLLT can be pointed as a promising therapeutic approach for lung inflammatory diseases as COPD.
Assuntos
Terapia com Luz de Baixa Intensidade/métodos , Pneumonia/terapia , Doença Pulmonar Obstrutiva Crônica/terapia , Animais , Modelos Animais de Doenças , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Receptores Purinérgicos P2X7/metabolismoRESUMO
PURPOSE: Obesity results in decreased lung function and increased inflammation. Moderate aerobic exercise (AE) reduced lung inflammation and remodeling in a variety of respiratory disease models. Therefore, this study investigated whether AE can attenuate a diet-induced obesity respiratory phenotype; including airway hyper-responsiveness (AHR), remodeling and inflammation. METHODS: Sixty C57Bl/6 male mice were distributed into four groups: control lean (CL), exercise lean (EL), obese (O) and obese exercise (OE) groups (2 sets of 7 and 8 mice per group; nâ¯=â¯15). A classical model of diet-induced obesity (DIO) over 12â¯weeks was used. AE was performed 60â¯min/day, 5â¯days/week for 5â¯weeks. Airway hyperresponsiveness (AHR), lung inflammation and remodeling, adipokines and cytokines in bronchoalveolar lavage (BAL) was determined. RESULTS: A high fat diet over 18â¯weeks significantly increased body weight (pâ¯<â¯.0001). Five weeks of AE significantly reduced both AHR and pulmonary inflammation. AHR in obese mice that exercised was reduced at the basal level (pâ¯<â¯.05), vehicle (PBS) (pâ¯<â¯.05), 6.25 MCh mg/mL (pâ¯<â¯.05), 12.5 MCh mg/mL (pâ¯<â¯.01), 25 MCh mg/mL (pâ¯<â¯.01) and 50 MCh mg/mL (pâ¯<â¯.05). Collagen (pâ¯<â¯.001) and elastic (pâ¯<â¯.001) fiber deposition in airway wall and also smooth muscle thickness (pâ¯<â¯.001) were reduced. The number of neutrophils (pâ¯<â¯.001), macrophages (pâ¯<â¯.001) and lymphocytes (pâ¯<â¯.01) were reduced in the peribronchial space as well as in the BAL: lymphocytes (pâ¯<â¯.01), macrophages (pâ¯<â¯.01), neutrophils (pâ¯<â¯.001). AE reduced obesity markers leptin (pâ¯<â¯.001), IGF-1 (pâ¯<â¯.01) and VEGF (pâ¯<â¯.001), while increased adiponectin (pâ¯<â¯.01) in BAL. AE also reduced pro-inflammatory cytokines in the BAL: IL-1ß (pâ¯<â¯.001), IL-12p40 (pâ¯<â¯.001), IL-13 (pâ¯<â¯.01), IL-17 (pâ¯<â¯.001, IL-23 (pâ¯<â¯.05) and TNF-alpha (pâ¯<â¯.05), and increased anti-inflammatory cytokine IL-10 (pâ¯<â¯.05). CONCLUSIONS: Aerobic exercise reduces high fat diet-induced obese lung phenotype (AHR, pulmonary remodeling and inflammation), involving anti-inflammatory cytokine IL-10 and adiponectin.