Effects of environmental exposure to iron powder on healthy and elastase-exposed mice.

Prolonged exposure to iron powder and other mineral dusts can threaten the health of individuals, especially those with COPD. The goal of this study was to determine how environmental exposure to metal dust from two different mining centers in Brazil affects lung mechanics, inflammation, remodeling and oxidative stress responses in healthy and elastase-exposed mice. This study divided 72 male C57Bl/6 mice into two groups, the summer group and the winter group. These groups were further divided into six groups: control, nonexposed (SAL); nonexposed, given elastase (ELA); exposed to metal powder at a mining company (SAL-L1 and ELA-L1); and exposed to a location three miles away from the mining company (SAL-L2 and ELA-L2) for four weeks. On the 29th day of the protocol, the researchers assessed lung mechanics, bronchoalveolar lavage fluid (BALF), inflammation, remodeling, oxidative stress, macrophage iron and alveolar wall alterations (mean linear intercept-Lm). The Lm was increased in the ELA, ELA-L1 and ELA-L2 groups compared to the SAL group (p < 0.05). There was an increase in the total number of cells and macrophages in the ELA-L1 and ELA-L2 groups compared to the other groups (p < 0.05). Compared to the ELA and SAL groups, the exposed groups (ELA-L1, ELA-L2, SAL-L1, and SAL-L2) exhibited increased expression of IL-1ß, IL-6, IL-10, IL-17, TNF-α, neutrophil elastase, TIMP-1, MMP-9, MMP-12, TGF-ß, collagen fibers, MUC5AC, iNOS, Gp91phox, NFkB and iron positive macrophages (p < 0.05). Although we did not find differences in lung mechanics across all groups, there were low to moderate correlations between inflammation remodeling, oxidative stress and NFkB with elastance, resistance of lung tissue and iron positive macrophages (p < 0.05). Environmental exposure to iron, confirmed by evaluation of iron in alveolar macrophages and in air, exacerbated inflammation, initiated remodeling, and induced oxidative stress responses in exposed mice with and without emphysema. Activation of the iNOS, Gp91phox and NFkB pathways play a role in these changes.

Physicians' attention to patients' communication cues can improve patient satisfaction with care and perception of physicians' empathy

ABSTRACT Background The pathway that links good communication skills and better health outcomes is still unclear. However, it is known that the way that physicians and patients communicate with each other has direct consequences on more "proximal outcomes", such as perceptions of physician empathy and patient satisfaction. However, which specific communication skills lead to those patient outcomes is still unknown. In this study, the authors aimed to analyze which specific patient and physician communication skills are correlated to patients' satisfaction with care and patient-perceived physician empathy. Methods The authors classified and quantified verbal and nonverbal communication of second-year internal medicine residents and their patients through video recordings of their consultations. Patients also rated their satisfaction with care and the physician's empathy for them. Results Using a linear regression model, the authors identified that patients' and physicians' expressions of disapproval, physicians' disruptions, and patients' use of content questions negatively correlated to patients' satisfaction and patient-perceived physician empathy. Conversely, patient affective behaviors and the physician's provision of advice/suggestion were positively correlated to at least one of the patient-measured outcomes. Conclusion Our findings point to the importance of physicians' attentiveness to patients' communication cues. Training physicians to interpret those cues could help develop more satisfactory and empathic therapeutic relationships.

Pedagogical concerns of physical therapist professors and their perceptions of the COVID-19 pandemic / Preocupaciones pedagógicas del fisioterapeuta-profesor y sus percepciones sobre la pandemia del COVID-19 / Preocupações pedagógicas do fisioterapeuta professor e suas percepções sobre a pandemia de COVID-19

ABSTRACT In health professions education, professors usually face some difficulties and concerns. The COVID-19 pandemic has further amplified these challenges, leading to changes in teaching methods and new concerns. This study aimed to identify undergraduate physical therapy professors' concerns (PC) about the learning environment during the COVID-19 pandemic. Physical therapists who served as undergraduate physical therapy professors in Brazil answered a questionnaire on PC (Teacher Concerns Questionnaire - TCQ), a sociodemographic profile questionnaire, and an open-ended question on the perception of changes in PC during the pandemic. A total of 187 physical therapist professors completed the questionary and had moderate PC (TCQ 49.6±10.5), with no association with the stage of their teaching career, age, and length of professional training. Participants in continuing education activities had higher PC. Of the participants, 94.1% reported changes in PC resulting from the pandemic. Therefore, professors who participate in continuing education activities are more concerned about the impact of their practice than those who do not participate. At the same time, these concerns seem to have changed during the pandemic.

RESUMEN En la formación de los profesionales de la salud, los docentes suelen experimentar algunas dificultades y preocupaciones. La pandemia del COVID-19 intensificó aún más estos desafíos, por provocar cambios en los métodos de enseñanza, dando lugar a nuevas preocupaciones. El objetivo de este estudio fue investigar las preocupaciones de los profesores (PP) de los cursos de graduación en Fisioterapia respecto al ambiente de aprendizaje durante la pandemia del COVID-19. Se invitó a fisioterapeutas que actuaban como profesores en cursos de graduación en Fisioterapia en Brasil a responder un cuestionario sobre las PP (Teacher Concerns Questionnaire, TCQ), sobre el perfil sociodemográfico y la percepción de cambios en PP en relación con la pandemia. Participaron 187 fisioterapeutas profesores que presentaron PP moderadas (TCQ: 49,6±10,5), sin asociación con la etapa de la carrera docente, la edad y el tiempo de formación profesional. Los participantes en actividades de formación continuada en la docencia tuvieron una PP más alta. El 94,1% de los participantes informaron cambios en PP resultantes de la pandemia. Se concluye que los profesores que participan en actividades de formación continuada están más preocupados por el impacto de su práctica. A la vez, estas preocupaciones parecen haber cambiado durante la pandemia.

RESUMO Na formação dos profissionais de saúde, os professores geralmente vivenciam algumas dificuldades e preocupações. A pandemia de COVID-19 amplificou ainda mais esses desafios, acarretando mudanças nos métodos de ensino e gerando novas preocupações. O objetivo deste estudo foi investigar quais são as preocupações dos professores (PPs) dos cursos de graduação em Fisioterapia com relação ao ambiente de aprendizagem durante a pandemia de COVID-19. Fisioterapeutas que atuavam como docentes em cursos de graduação em Fisioterapia no Brasil foram convidados a responder a um questionário de sobre as PPs (Teacher Concerns Questionnaire - TCQ), sobre perfil sociodemográfico e sobre a percepção de mudanças nas PPs devido à pandemia. Participaram 187 fisioterapeutas professores que apresentaram PP moderada (TCQ: 49,6±10,5), sem associação com a fase da carreira docente, a idade ou o tempo de formação. Aqueles que participam de atividades de formação continuada em docência apresentaram maior PP. Alterações nas PPs decorrentes da pandemia foram relatadas por 94,1% dos participantes. Conclui-se que os professores que participam de atividades de formação continuada se preocupam mais com o impacto de sua prática do que os que não participam. Ao mesmo tempo, essas preocupações parecem ter mudado durante a pandemia.

Aerobic exercise training engages cholinergic signaling to improve emphysema induced by cigarette smoke exposure in mice.

Lung inflammation is modulated by cholinergic signaling and exercise training protects mice against pulmonary emphysema development; however, whether exercise training engages cholinergic signaling is unknown. AIMS: As cholinergic signaling is directly linked to the vesicular acetylcholine transporter (VAChT) levels, we evaluated whether the effects of aerobic exercise training depend on the VAChT levels in mice with pulmonary emphysema. MAIN METHODS: Wild-type (WT) and mutant (KDHOM) mice (65-70% of reduction in VAChT levels) were exposed to cigarette smoke (30 min, 2×/day, 5×/week, 12 weeks) and submitted or not to aerobic exercise training on a treadmill (60 min/day, 5×/week, 12 weeks). Lung function and inflammation were evaluated. KEY FINDINGS: Cigarette smoke reduced body mass in mice (p < 0.001) and increased alveolar diameter (p < 0.001), inflammation (p < 0.001) and collagen deposition (p < 0.01) in lung tissue. Both trained groups improved their performance in the final physical test compared to the initial test (p < 0.001). In WT mice, exercise training protected against emphysema development (p < 0.05), reduced mononuclear cells infiltrate (p < 0.001) and increased MAC-2 positive cells in lung parenchyma (p < 0.05); however, these effects were not observed in KDHOM mice. The exercise training reduced iNOS-positive cells (p < 0.001) and collagen fibers deposition (p < 0.05) in lung parenchyma of WT and KDHOM mice, although KDHOM mice showed higher levels of iNOS-positive cells. SIGNIFICANCE: Our data suggest that the protective effects of aerobic exercise training on pulmonary emphysema are, at least in part, dependent on the integrity of the lung cholinergic signaling.

Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model.

Chronic exposure to ambient levels of air pollution induces respiratory illness exacerbation by increasing inflammatory responses and apoptotic cells in pulmonary tissues. The ineffective phagocytosis of these apoptotic cells (efferocytosis) by macrophages has been considered an important factor in these pathological mechanisms. Depending on microenvironmental stimuli, macrophages can assume different phenotypes with different functional actions. M1 macrophages are recognized by their proinflammatory activity, whereas M2 macrophages play pivotal roles in responding to microorganisms and in efferocytosis to avoid the progression of inflammatory conditions. To verify how exposure to air pollutants interferes with macrophage polarization in emphysema development, we evaluated the different macrophage phenotypes in a PPE- induced model with the exposure to diesel exhaust particles. C57BL/6 mice received intranasal instillation of porcine pancreatic elastase (PPE) to induce emphysema, and the control groups received saline. Both groups were exposed to diesel exhaust particles or filtered air for 60 days according to the groups. We observed that both the diesel and PPE groups had an increase in alveolar enlargement, collagen and elastic fibers in the parenchyma and the number of macrophages, lymphocytes and epithelial cells in BAL, and these responses were exacerbated in animals that received PPE instillation prior to exposure to diesel exhaust particles. The same response pattern was found inCaspase-3 positive cell analysis, attesting to an increase in cell apoptosis, which is in agreement with the increase in M2 phenotype markers, measured by RT-PCR and flow cytometry analysis. We did not verify differences among the groups for the M1 phenotype. In conclusion, our results showed that both chronic exposure to diesel exhaust particles and PPE instillation induced inflammatory conditions, cell apoptosis and emphysema development, as well as an increase in M2 phenotype macrophages, and the combination of these two factors exacerbated these responses. The predominance of the M2-like phenotype likely occurred due to the increased demand for efferocytosis. However, M2 macrophage activity was ineffective, resulting in emphysema development and worsening of symptoms.

The deleterious effects of smoking in bone mineralization and fibrillar matrix composition.

INTRODUCTION: This study aimed to verify the effects of cigarette smoke exposure in bone mineralization and fibrillar matrix composition as well as in bone healing after tibial fracture induction. METHODS: C57Bl/6 Mice were assigned according to exposure and surgery: C room air; F room air and tibia open osteotomy; CS cigarette smoke; FCS cigarette smoke and tibia open osteotomy. In order to study fracture healing we performed, under anesthesia, a bone injury through a tibial shaft osteotomy. Bone samples were obtained to evaluate bone histomorphometry, trabecular morphology and volume, trabecular collagen types composition and presence of inflammatory cytokines and growth factors. RESULTS: CS exposure significantly reduced the thickness of bone trabeculae associated with decrease in mineralizing surface and mineral deposition rate, leading a lower bone formation rate and longer mineralization time. Resorption surface and osteoclastic surface were greater in the CS group, attesting increased resorptive action. There was a decrease in type I collagen deposition and genes expression in the CS and FCS groups compared to C group and in contrast there was an increase in type V collagen deposition and genes expression in the CS, FC and FSC groups compared to C group. Also, CS exposure induced a decrease in bone forming cytokines and an increase in inflammatory associated cytokines, and these changes were intensified under fracture conditions. CONCLUSION: Cigarette smoke exposure alters bone matrix composition and worsens bone mineralization, leading to bone fragility by increasing collagen V synthesis and deposition and impairing collagen I fibril forming and assembling. And these deleterious effects contributed to the worsening in fracture healing after tibia osteotomy.

Physical Exercise Induces Immunoregulation of TREG, M2, and pDCs in a Lung Allergic Inflammation Model.

The benefits of moderate aerobic physical exercise for allergic asthma are well-known, particularly that of the anti-inflammatory effect that occurs by reducing Th2 responses and lung remodeling. However, the mechanisms of this immunoregulation are still under investigation. In this study, we investigated the possible immunoregulatory mechanisms of lung inflammation induced by moderate aerobic exercise in an experimental asthma model. BALB/c mice were distributed into Control, Exercise (EX), OVA, and OEX groups. OVA and OEX groups were sensitized with ovalbumin (OVA) on days 0, 14, 21, 28, and 42 and were challenged with OVA aerosol three times a week from days 21 to 51. The EX and OEX groups underwent moderate aerobic physical exercise from days 21 to 51 (5 d/w, 1 h/d). The mice were euthanized on day 52. We evaluated pulmonary cytokine production, serum immunoglobulin levels, and the inflammatory cell profile in lung and mediastinal lymph nodes. OVA mice showed increased expression of IL-4, IL-6, IL-10, and TGF-ß and decreased macrophage type 2 (M2) recruitment. Physical exercise did not affect the increased antibody production of IgG2a, IgG1, or IgE induced by OVA. Of note, physical exercise alone markedly increased production of anti-inflammatory cytokines such as IL-10 and TGF-ß. Physical exercise in OVA-mice also increased the recruitment of M2 in the lungs, as well as the influx and activation of regulatory T cells (Tregs) and CD4 and CD8 lymphocytes. In the draining lymph nodes, it was also observed that physical exercise increased the activation of CD4 T cells, regardless of the presence of OVA. Notably, physical exercise decreased common dendritic cells' (cDCs; pro-inflammatory) expression of co-stimulatory molecules such as CD80, CD86, and ICOSL in the draining lymph nodes, as well as increased ICOSL in plasmacytoid dendritic cells (pDCs; anti-inflammatory). Together, these findings show that physical exercise modulates pulmonary allergic inflammation by increasing Treg and M2 recruitment, as well as pDCs activation, which leads to an increase in anti-inflammatory cytokines and a decrease in pro-inflammatory cells and mediators.

A possible association between fructose consumption and pulmonary emphysema.

Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary fibers, fruits and vegetables intake protects against the COPD development, while fructose-loading is associated with increased risk of asthma and chronic bronchitis. Since dietary factors might affect susceptibility to COPD by modulating oxidative stress and inflammatory responses, we evaluated how fructose feeding might affect the smoking-induced emphysema in mice. We found that chronic fructose intake induced destruction and remodeling of lung parenchyma and impairment of respiratory mechanics, which are associated with distinctive cytokine profiles in bronchoalveolar lavage fluid, blood plasma and skeletal muscle. The combined effects of chronic fructose intake and cigarette smoking on destruction of lung parenchyma are more pronounced than the effects of either alone. Excessive intake of fructose might directly cause pulmonary emphysema in mice rather than just altering its natural history by facilitating the installation of a low-grade systemic inflammatory milieu.

A murine model of elastase- and cigarette smoke-induced emphysema.

OBJECTIVE:: To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS) and instillation of porcine pancreatic elastase (PPE). METHODS:: A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution); PPE (two intranasal instillations of PPE); CS (CS exposure for 60 days); and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days). At the end of the experimental protocol, all animals were anesthetized and tracheostomized for calculation of respiratory mechanics parameters. Subsequently, all animals were euthanized and their lungs were removed for measurement of the mean linear intercept (Lm) and determination of the numbers of cells that were immunoreactive to macrophage (MAC)-2 antigen, matrix metalloproteinase (MMP)-12, and glycosylated 91-kDa glycoprotein (gp91phox) in the distal lung parenchyma and peribronchial region. RESULTS:: Although there were no differences among the four groups regarding the respiratory mechanics parameters assessed, there was an increase in the Lm in the CS + PPE group. The numbers of MAC-2-positive cells in the peribronchial region and distal lung parenchyma were higher in the CS + PPE group than in the other groups, as were the numbers of cells that were positive for MMP-12 and gp91phox, although only in the distal lung parenchyma. CONCLUSIONS:: Our model of emphysema induced by a combination of PPE instillation and CS exposure results in a significant degree of parenchymal destruction in a shorter time frame than that employed in other models of CS-induced emphysema, reinforcing the importance of protease-antiprotease imbalance and oxidant-antioxidant imbalance in the pathogenesis of emphysema. OBJETIVO:: Descrever um modelo murino de enfisema induzido por exposição a fumaça de cigarro (FC) e instilação de elastase pancreática porcina (EPP). MÉTODOS:: Trinta e oito camundongos C57BL/6 foram aleatoriamente divididos em quatro grupos: controle (uma instilação intranasal de solução salina a 0,9%); EPP (duas instilações intranasais de EPP); FC (exposição a FC durante 60 dias) e FC + EPP (duas instilações intranasais de EPP + exposição a FC durante 60 dias). No fim do protocolo experimental, todos os animais foram anestesiados e traqueostomizados para o cálculo de parâmetros de mecânica respiratória. Em seguida, todos os animais foram sacrificados e seus pulmões foram removidos para a medição da intercepção linear média (Lm) e a determinação do número de células imunorreativas a antígeno macrofágico (MAC)-2, metaloproteinase da matriz (MMP)-12 e glicoproteína glicosilada de 91 kDa (gp91phox) no parênquima pulmonar distal e na região peribrônquica. RESULTADOS:: Embora não tenha havido diferenças entre os quatro grupos quanto aos parâmetros de mecânica respiratória avaliados, houve aumento da Lm no grupo FC + EPP. O número de células positivas para MAC-2 na região peribrônquica e no parênquima pulmonar distal foi maior no grupo FC + EPP do que nos outros grupos, assim como o foi o número de células positivas para MMP-12 e gp91phox, porém somente no parênquima pulmonar distal. CONCLUSÕES:: Nosso modelo de enfisema induzido por instilação de EPP e exposição a FC resulta em um grau significativo de destruição parenquimatosa em um período de tempo menor que o empregado em outros modelos de enfisema induzido por FC, o que reforça a importância do desequilíbrio entre proteases e antiproteases e entre oxidantes e antioxidantes na patogênese do enfisema.

A murine model of elastase- and cigarette smoke-induced emphysema / Modelo murino de enfisema induzido por instilação de elastase e exposição a fumaça de cigarro

ABSTRACT Objective: To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS) and instillation of porcine pancreatic elastase (PPE). Methods: A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution); PPE (two intranasal instillations of PPE); CS (CS exposure for 60 days); and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days). At the end of the experimental protocol, all animals were anesthetized and tracheostomized for calculation of respiratory mechanics parameters. Subsequently, all animals were euthanized and their lungs were removed for measurement of the mean linear intercept (Lm) and determination of the numbers of cells that were immunoreactive to macrophage (MAC)-2 antigen, matrix metalloproteinase (MMP)-12, and glycosylated 91-kDa glycoprotein (gp91phox) in the distal lung parenchyma and peribronchial region. Results: Although there were no differences among the four groups regarding the respiratory mechanics parameters assessed, there was an increase in the Lm in the CS + PPE group. The numbers of MAC-2-positive cells in the peribronchial region and distal lung parenchyma were higher in the CS + PPE group than in the other groups, as were the numbers of cells that were positive for MMP-12 and gp91phox, although only in the distal lung parenchyma. Conclusions: Our model of emphysema induced by a combination of PPE instillation and CS exposure results in a significant degree of parenchymal destruction in a shorter time frame than that employed in other models of CS-induced emphysema, reinforcing the importance of protease-antiprotease imbalance and oxidant-antioxidant imbalance in the pathogenesis of emphysema.

RESUMO Objetivo: Descrever um modelo murino de enfisema induzido por exposição a fumaça de cigarro (FC) e instilação de elastase pancreática porcina (EPP). Métodos: Trinta e oito camundongos C57BL/6 foram aleatoriamente divididos em quatro grupos: controle (uma instilação intranasal de solução salina a 0,9%); EPP (duas instilações intranasais de EPP); FC (exposição a FC durante 60 dias) e FC + EPP (duas instilações intranasais de EPP + exposição a FC durante 60 dias). No fim do protocolo experimental, todos os animais foram anestesiados e traqueostomizados para o cálculo de parâmetros de mecânica respiratória. Em seguida, todos os animais foram sacrificados e seus pulmões foram removidos para a medição da intercepção linear média (Lm) e a determinação do número de células imunorreativas a antígeno macrofágico (MAC)-2, metaloproteinase da matriz (MMP)-12 e glicoproteína glicosilada de 91 kDa (gp91phox) no parênquima pulmonar distal e na região peribrônquica. Resultados: Embora não tenha havido diferenças entre os quatro grupos quanto aos parâmetros de mecânica respiratória avaliados, houve aumento da Lm no grupo FC + EPP. O número de células positivas para MAC-2 na região peribrônquica e no parênquima pulmonar distal foi maior no grupo FC + EPP do que nos outros grupos, assim como o foi o número de células positivas para MMP-12 e gp91phox, porém somente no parênquima pulmonar distal. Conclusões: Nosso modelo de enfisema induzido por instilação de EPP e exposição a FC resulta em um grau significativo de destruição parenquimatosa em um período de tempo menor que o empregado em outros modelos de enfisema induzido por FC, o que reforça a importância do desequilíbrio entre proteases e antiproteases e entre oxidantes e antioxidantes na patogênese do enfisema.

Comparison of the effects of aerobic conditioning before and after pulmonary allergic inflammation.

The aim of this study is to compare the effects of aerobic conditioning (AC) before (ACBS) and after (ACAS) allergic sensitization. BALB/c mice were divided into two main groups: ACBS and ACAS. Each groups was divided into subgroups: control (nonsensitized/nontrained), AC (nonsensitized/trained), ovalbumin (OVA) (sensitized/nontrained), AC+OVA (trained/sensitized), and OVA+AC (sensitized/trained). Sensitization was induced using OVA and AC performed in treadmill (moderate intensity). We examined IgE and IgG1 levels, eosinophil counting, expression of Th1 (interleukin (IL)-2, IFN-α) and Th2 cytokines (IL-4, IL-5, IL-13), IL-10, vascular endothelial growth factor (VEGF), and airway remodeling. IgE and IgG1 were decreased only when exercise was performed before sensitization (ACBS); however, there was a decrease of eosinophils, Th2 cytokines, VEGF, and airway remodeling and increase in IL-10 in either ACBS or ACAS groups. Our results demonstrate that aerobic conditioning reduces Th2 response before and after sensitization by increasing IL-10 while the production of anaphylactic antibodies is reduced only when exercise is performed before sensitization.

O exercício aeróbio atenua a inflamação pulmonar induzida pelo Streptococcus pneumoniae / Aerobic exercise attenuates pulmonary inflammation induced by Streptococcus pneumoniae

O treinamento aeróbio moderado tem sido reconhecido como um importante estimulador do sistema imune, no entanto o efeito deste na infecção bacteriana não tem sido extensivamente estudado. Nosso objetivo foi avaliar se o exercício aeróbio moderado prévio à infecção por S. pneumoniae influencia a resposta inflamatória pulmonar. Camundongos BALB/C foram divididos em 4 grupos: Controle (animais sedentários; não infectados); S. pneumoniae (animais sedentários e posteriormente infectados); Exercício (animais treinados; não infectados); Exercício + S. pneumoniae (animais treinados e posteriormente infectados). Os animais foram submetidos a um programa de treinamento físico aeróbio durante 4 semanas, e 72 horas após a última sessão de exercício, os animais receberam instilação nasal de S. pneumoniae (linhagem M10) e foram avaliados 12 horas (fase aguda) ou 10 dias (fase tardia) após a instilação. Na fase aguda, o grupo S. pneumoniae apresentou um aumento de: resistência e elastância do sistema respiratório, número total de células, neutrófilos, linfócitos e macrófagos no lavado broncoalveolar (BAL), células polimorfonucleares no parênquima pulmonar e TNF-alfa e IL-1beta no homogenato pulmonar. O exercício físico atenuou significantemente esses parâmentros. Além disso, o exercício físico resultou em aumento da expressão de enzimas antioxidantes no pulmão (CuZnSOD and MnSOD). Na fase tardia, o grupo Exercício + S. pneumoniae apresentou redução no número total de células e macrófagos no BAL, células polimorfonucleares no parênquima pulmonar e IL-6 no homogenato pulmonar comparado ao grupo S. pneumoniae. Nossos resultados sugerem um efeito protetor do exercício aeróbio moderado contra a infecção bacteriana pulmonar. Esse efeito é provavelmente secundário ao efeito do exercício no balanço oxidante-antioxidante.

Moderate aerobic exercise training has been recognized as an important stimulator of the immune system, but its effect on bacterial infection has not been extensively studied. Our aim was to determine whether moderate aerobic exercise training prior to S. pneumoniae infection influences pulmonary inflammatory responses. BALB/c mice were divided into 4 groups: Control (sedentary without infection); S. pneumoniae (sedentary with infection); Exercise (aerobic training without infection); Exercise + S. pneumoniae (aerobic training with infection). Animals underwent aerobic exercise training for 4 weeks. 72 h after last exercise training, animals received a challenge with S. pneumoniae (strain M10) and were evaluated either 12 h (acute phase) or 10 days (late phase) after instillation. In acute phase, S. pneumoniae group had an increase in respiratory system resistance and elastance; number of total cells, neutrophils, lymphocytes and macrophages in bronchoalveolar lavage fluid (BAL); polymorphonuclear cells in lung parenchyma; and levels of TNF-alfa and IL-1beta in lung homogenates. Exercise training significantly attenuated the increase in all of these parameters. In addition, exercise induced an increase in expression of antioxidant enzymes (CuZnSOD and MnSOD) in lungs. In late phase, Exercise + S. pneumoniae group exhibited a reduction in number of total cells and macrophages in BAL, in polymorphonuclear cells in lung parenchyma and in levels of IL-6 in lung homogenates compared to S. pneumoniae group. Our results suggest a protective effect of moderate exercise training against respiratory infection with S. pneumoniae. This effect is most likely secondary to an effect of exercise on oxidant-antioxidant balance.

Anti-inflammatory effects of aerobic exercise in mice exposed to air pollution.

PURPOSE: Exposure to diesel exhaust particles (DEP) results in lung inflammation. Regular aerobic exercise improves the inflammatory status in different pulmonary diseases. However, the effects of long-term aerobic exercise on the pulmonary response to DEP have not been investigated. The present study evaluated the effect of aerobic conditioning on the pulmonary inflammatory and oxidative responses of mice exposed to DEP. METHODS: BALB/c mice were subjected to aerobic exercise five times per week for 5 wk, concomitantly with exposure to DEP (3 mg·mL(-1); 10 µL per mouse). The levels of exhaled nitric oxide, reactive oxygen species, cellularity, interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) were analyzed in bronchoalveolar lavage fluid, and the density of neutrophils and the volume proportion of collagen fibers were measured in the lung parenchyma. The cellular density of leukocytes expressing IL-1ß, keratinocyte chemoattractant (KC), and TNF-α in lung parenchyma was evaluated with immunohistochemistry. The levels of IL-1ß, KC, and TNF-α were also evaluated in the serum. RESULTS: Aerobic exercise inhibited the DEP-induced increase in the levels of reactive oxygen species (P < 0.05); exhaled nitric oxide (P < 0.01); total (P < 0.01) and differential cells (P < 0.01); IL-6 and TNF-α levels in bronchoalveolar lavage fluid (P < 0.05); the level of neutrophils (P < 0.001); collagen density in the lung parenchyma (P < 0.05); the levels of IL-6, KC, and TNF-α in plasma (P < 0.05); and the expression of IL-1ß, KC, and TNF-α by leukocytes in the lung parenchyma (P < 0.01). CONCLUSIONS: We conclude that long-term aerobic exercise presents protective effects in a mouse model of DEP-induced lung inflammation. Our results indicate a need for human studies that evaluate the pulmonary responses to aerobic exercise chronically performed in polluted areas.

Respiratory mechanics do not always mirror pulmonary histological changes in emphysema.

OBJECTIVE: To verify the accordance of functional and morphometric parameters during the development of emphysema. METHODS: BALB/c mice received a nasal drop of either papain or saline solution and were studied after 1, 3, 15, 28, and 40 days. Functional parameters, such as airway resistance, tissue damping, and tissue elastance, were analyzed. To evaluate the structural changes and possible mechanisms involved in this disease, we measured the mean linear intercept, the volume proportions of elastic and collagen fibers, the number of macrophages, the numbers of cells expressing metalloprotease 12 and 8-isoprostane in lung parenchyma. RESULTS: We only observed decreases in tissue elastance and tissue damping on the 28th day, with a concomitant increase in the mean linear intercept, indicating the presence of emphysema. However, only the mean linear intercept values remained increased until the 40th day. The volume proportion of collagen fibers was increased from the 15th day to the 40th day, whereas the volume proportion of elastic fibers was only increased on the 40th day. The number of macrophages increased beginning on the 1st day. The expression of metalloproteinase 12 was increased from the 3rd day until the 40th day. However, 8-isoprostane expression was only increased on the 1st and 3rd days. CONCLUSIONS: In this study, morphometric parameters were found to be more reliable for detecting the presence of emphysema than the functional parameters measured by respiratory mechanics. Further investigations are necessary to understand how the extracellular matrix remodeling observed in the lung parenchyma could be involved in this process.

Respiratory mechanics do not always mirror pulmonary histological changes in emphysema

OBJECTIVE: To verify the accordance of functional and morphometric parameters during the development of emphysema. METHODS: BALB/c mice received a nasal drop of either papain or saline solution and were studied after 1, 3, 15, 28, and 40 days. Functional parameters, such as airway resistance, tissue damping, and tissue elastance, were analyzed. To evaluate the structural changes and possible mechanisms involved in this disease, we measured the mean linear intercept, the volume proportions of elastic and collagen fibers, the number of macrophages, the numbers of cells expressing metalloprotease 12 and 8-isoprostane in lung parenchyma. RESULTS: We only observed decreases in tissue elastance and tissue damping on the 28th day, with a concomitant increase in the mean linear intercept, indicating the presence of emphysema. However, only the mean linear intercept values remained increased until the 40th day. The volume proportion of collagen fibers was increased from the 15th day to the 40th day, whereas the volume proportion of elastic fibers was only increased on the 40th day. The number of macrophages increased beginning on the 1st day. The expression of metalloproteinase 12 was increased from the 3rd day until the 40th day. However, 8-isoprostane expression was only increased on the 1st and 3rd days. CONCLUSIONS: In this study, morphometric parameters were found to be more reliable for detecting the presence of emphysema than the functional parameters measured by respiratory mechanics. Further investigations are necessary to understand how the extracellular matrix remodeling observed in the lung parenchyma could be involved in this process.