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1.
Medicine (Baltimore) ; 99(7): e19118, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32049827

RESUMO

Cigarette smoking is considered the main risk factor for chronic obstructive pulmonary disease (COPD), although the mechanism remains unknown. surfactant protein A (SP-A) is thought to protect the lung from smoking-induced damage, but related studies performed in China are scarce. The aim of the study is to assess alterations of SP-A expression and distribution in lung samples from Chinese smokers with or without COPD.This cross-sectional study assessed 45 men in Wuhan Tongji Hospital after lobectomy for lung cancer in June 2010 to September 2010. Peripheral lung specimens were collected from control nonsmokers without airflow obstruction (nonsmoking group, n = 15), smokers without airflow obstruction (smoking group, n = 15), and patients with COPD (COPD group, n = 15). SP-A expression levels in lung tissue samples and its distribution in lung cells, type II pneumocytes (PNII), and alveolar macrophages (MACR) were determined by immunoblotting and immunohistochemistry.SP-A levels were significantly decreased in the COPD group (1.00 ±â€Š0.25) compared with the smoking (2.31 ±â€Š0.64) and nonsmoking (8.03 ±â€Š2.80) groups; the smoking group also showed significantly reduced levels compared with the nonsmoking group (P < .05). PNII expressing SP-A were less abundant in the COPD group (39.3% ±â€Š7.1%) compared with the smoking group (76.2% ±â€Š29.8%), whereas SP-A MACR were more abundant (92.4% ±â€Š7.1% vs 68.5% ±â€Š20.2%) (all P < .05). Among the 30 smokers, forced expiratory volume in one second (% predicted) was positively correlated with SP-A levels (r = 0.739) and the rate of SP-A+ PNII (r = 0.811), and negatively correlated with the rate of SP-A+ MACR (r = -0.758) (all P < .05).Changes in SP-A expression and distribution in lung tissues may be involved in COPD pathogenesis in smokers.


Assuntos
Doença Pulmonar Obstrutiva Crônica/genética , Proteína A Associada a Surfactante Pulmonar/metabolismo , Fumar/efeitos adversos , Idoso , Estudos de Casos e Controles , China , Estudos Transversais , Volume Expiratório Forçado , Humanos , Pulmão/patologia , Masculino , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/etiologia , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Fumantes/estatística & dados numéricos
2.
J Ethnopharmacol ; 247: 112259, 2020 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-31577938

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Ximenia americana L. is popularly known as yellow plum, brave plum or tallow wood. All the parts of this plant are used in popular medicine. Its reddish and smooth bark are used to treat skin infections, inflammation of the mucous membranes and in the wound healing process. OBJECTIVE: Verification of phytochemical profile, the molecular interaction between flavonoid, (-) epi-catechin and 5-LOX enzyme, by means of in silico study, the genotoxic effect and to investigate the pharmacological action of the aqueous extract of the stem bark of X. americana in pulmonary alterations caused by experimental COPD in Rattus norvegicus. MATERIALS AND METHODS: The identification of secondary metabolites was carried out by TLC and HPLC chromatographic methods, molecular anchoring tests were applied to analyze the interaction of flavonoid present in the extract with the enzyme involved in pulmonary inflammation process and the genotoxic effect was assessed by comet assay and micronucleus test. For induction of COPD, male rats were distributed in seven groups. The control group was exposed only to ambient air and six were subjected to passive smoke inhalations for 20 min/day for 60 days. One of the groups exposed to cigarette smoke did not receive treatment. The others were treated by inhalation with beclomethasone dipropionate (400 mcg/kg) and aqueous and lyophilized extracts of X. americana (500 mg/kg) separately or in combination for a period of 15 days. The structural and inflammatory pulmonary alterations were evaluated by histological examination. Additional morphometric analyses were performed, including the alveolar diameter and the thickness of the right ventricle wall. RESULTS: The results showed that the aqueous extract of the bark of X. americana possesses (-) epi -catechin, in silico studies with 5-LOX indicate that the EpiC ligand showed better affinity parameters than the AracA ligand, which is in accordance with the results obtained in vivo studies. Genotoxity was not observed at the dose tested and the extract was able to stagnate the alveolar enlargement caused by the destruction of the interalveolar septa, attenuation of mucus production and decrease the presence of collagen fibers in the bronchi of animals submitted to cigarette smoke. CONCLUSION: Altogether, the results proved that the aqueous extract of X. americana presents itself as a new option of therapeutic approach in the treatment of COPD.


Assuntos
Dano ao DNA/efeitos dos fármacos , Inibidores de Lipoxigenase/farmacologia , Olacaceae/química , Extratos Vegetais/farmacologia , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Animais , Araquidonato 5-Lipoxigenase/química , Araquidonato 5-Lipoxigenase/farmacologia , Brasil , Modelos Animais de Doenças , Etnofarmacologia , Feminino , Humanos , Inibidores de Lipoxigenase/química , Inibidores de Lipoxigenase/isolamento & purificação , Inibidores de Lipoxigenase/uso terapêutico , Masculino , Simulação de Acoplamento Molecular , Testes de Mutagenicidade , Casca de Planta/química , Extratos Vegetais/química , Extratos Vegetais/isolamento & purificação , Extratos Vegetais/uso terapêutico , Caules de Planta/química , Doença Pulmonar Obstrutiva Crônica/etiologia , Ratos , Ratos Wistar , Poluição por Fumaça de Tabaco/efeitos adversos , Resultado do Tratamento
4.
Lakartidningen ; 1162019 Nov 26.
Artigo em Sueco | MEDLINE | ID: mdl-31769860

RESUMO

Occupational exposures to gas, fumes, dust and chemicals contribute to non-malignant respiratory diseases like asthma, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and community-acquired pneumonia in more than one in ten patients. They may be sick due to inhaling various particles, gases, fumes, or chemicals in the workplace. Hence, these exposures should be considered in all patients with non-malignant respiratory diseases. In an international literature review the occupational burden of asthma was 16%, chronic obstructive pulmonary disease 14%, idiopathic pulmonary fibrosis 26% and community-acquired pneumonia 10%.


Assuntos
Exposição por Inalação/efeitos adversos , Exposição Ocupacional/efeitos adversos , Doenças Respiratórias/etiologia , Alveolite Alérgica Extrínseca/etiologia , Asma/etiologia , Bronquite Crônica/etiologia , Humanos , Doenças Profissionais/etiologia , Pneumonia/etiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Fibrose Pulmonar/etiologia , Sarcoidose/etiologia
5.
Toxicol Lett ; 317: 92-101, 2019 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-31593750

RESUMO

Cigarette smoke (CS) is known to cause mitochondrial dysfunction leading to cellular senescence in lung cells. We determined the mechanism of mitochondrial dysfunction by CS in lung epithelial cells. CS extract (CSE) treatment differentially affected mitochondrial function, such as membrane potential, mitochondrial reactive oxygen species (mtROS) and mitochrondrial mass as analyzed by FACS, and were associated with altered oxidative phosphorylation (OXPHOS) protein levels (Complexes I-IV) in primary lung epithelial cells (SAEC and NHBE), and (complexes I and II) in BEAS2B cells. There were dose- and time-dependent changes in mitochondrial respiration (oxygen consumption rate parameters i.e. maximal respiration, ATP production and spare capacity, measured by the Seahorse analyzer) in control vs. CSE treated BEAS2B and NHBE/DHBE cells. Electron microscopy (EM) analysis revealed perinuclear clustering by localization and increased mitochondrial fragmentation by fragement length analysis. Immunoblot analysis revealed CS-mediated increase in Drp1 and decrease in Mfn2 levels that are involved in mitochondrial fission/fusion process. CSE treatment reduced Miro1 and Pink1 abundance that play a crucial role in the intercellular transfer mechanism and mitophagy process. Overall, these findings highlight the role of Miro1 in context of CS-induced mitochondrial dysfunction in lung epithelial cells that may contribute to the pathogenesis of chronic inflammatory lung diseases.


Assuntos
Fumar Cigarros/efeitos adversos , Células Epiteliais/metabolismo , Pulmão/metabolismo , Mitocôndrias/metabolismo , Proteínas Mitocondriais/metabolismo , Doença Pulmonar Obstrutiva Crônica/etiologia , Fumaça/efeitos adversos , Proteínas rho de Ligação ao GTP/metabolismo , Estudos de Casos e Controles , Células Cultivadas , Regulação para Baixo , Metabolismo Energético , Células Epiteliais/ultraestrutura , Humanos , Pulmão/ultraestrutura , Mitocôndrias/ultraestrutura , Estresse Oxidativo , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/patologia , Transdução de Sinais
6.
Artigo em Inglês | MEDLINE | ID: mdl-31623202

RESUMO

The use of electronic cigarettes (e-cigarettes) has increased in the US, but little is known about the effects of these products on lung health. The main purpose of this study was to examine the association between e-cigarette use and a participant's report of being diagnosed with chronic obstructive pulmonary disease (COPD) in a nationally representative sample of adults. Methods: The first wave of the Population Assessment of Tobacco and Health (PATH) survey adult data was used (N = 32,320). Potential confounders between e-cigarette users and non-users were balanced using propensity score matching. Odds ratios (OR) were calculated to examine the association between e-cigarette use and COPD in the propensity-matched sample, the entire sample, different age groups, and in nonsmokers. Replicate weights and balanced repeated replication methods were utilized to account for the complex survey design. Results: Of the 3642 participants who met the criteria for e-cigarette use, 2727 were propensity matched with 2727 non e-cigarette users. In the propensity-matched sample, e-cigarette users were more likely to report being diagnosed with COPD (OR 1.43, 95% confidence interval [CI] 1.12-1.85) than non-e-cigarette users after adjusting for confounders. The result was similar in the entire sample and in the different age subgroups. Among nonsmokers, the odds of reporting a COPD diagnosis were even greater among e-cigarette users (OR 2.94, 95% CI 1.73-4.99) compared to non-e-cigarette users. Conclusion: Our findings demonstrate that e-cigarette use was associated with a reported diagnosis of COPD among adults in the US. Further research is necessary to characterize the nature of this association and on the long-term effects of using e-cigarettes.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Doença Pulmonar Obstrutiva Crônica/etiologia , Vaping/efeitos adversos , Adolescente , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Autorrelato , Produtos do Tabaco/estatística & dados numéricos , Adulto Jovem
7.
Environ Int ; 133(Pt A): 105164, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31518939

RESUMO

INTRODUCTION: Fuel poverty affects up to 35% of European homes, which represents a significant burden on society and healthcare systems. Draught proofing homes to prevent heat loss, improved glazing, insulation and heating (energy efficiency measures) can make more homes more affordable to heat. This has prompted significant investment in energy efficiency upgrades for around 40% of UK households to reduce the impact of fuel poverty. Despite some inconsistent evidence, household energy efficiency interventions can improve cardiovascular and respiratory health outcomes. However, the health benefits of these interventions have not been fully explored; this is the focus of this study. METHODS: In this cross sectional ecological study, we conducted two sets of analyses at different spatial resolution to explore population data on housing energy efficiency measures and hospital admissions at the area-level (counts grouped over a 3-year period). Housing data were obtained from three data sets covering housing across England (Household Energy Efficiency Database), Energy Performance Certificate (EPC) and, in the South West of England, the Devon Home Analytics Portal. These databases provided data aggregated to Lower Area Super Output Area and postcode level (Home Analytics Portal only). These datasets provided measures of both state (e.g. EPC ratings) and intervention (e.g. number of boiler replacements), aggregated spatially and temporally to enable cross-sectional analyses with health outcome data. Hospital admissions for adult (over 18 years) asthma, chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) were obtained from the Hospital Episode Statistics database for the national (1st April 2011 to 31st March 2014) and Devon, South West of England (1st April 2014 to 31st March 2017) analyses. Descriptive statistics and regression models were used to describe the associations between small area household energy efficiency measures and hospital admissions. Three main analyses were undertaken to investigate the relationships between; 1) household energy efficiency improvements (i.e. improved glazing, insulation and boiler upgrades); 2) higher levels of energy efficiency ratings (measured by Energy Performance Certificate ratings); 3) energy efficiency improvements and ratings (i.e. physical improvements and rating assessed by the Standard Assessment Procedure) and hospital admissions. RESULTS: In the national analyses, household energy performance certificate ratings ranged from 37 to 83 (mean 61.98; Standard Deviation 5.24). There were a total of 312,837 emergency admissions for asthma, 587,770 for COPD and 839,416 for CVD. While analyses for individual energy efficiency metrics (i.e. boiler upgrades, draught proofing, glazing, loft and wall insulation) were mixed; a unit increase in mean energy performance rating was associated with increases of around 0.5% in asthma and CVD admissions, and 1% higher COPD admission rates. Admission rates were also influenced by the type of dwelling, tenure status (e.g. home owner versus renting), living in a rural area, and minimum winter temperature. DISCUSSION: Despite a range of limitations and some mixed and contrasting findings across the national and local analyses, there was some evidence that areas with more energy efficiency improvements resulted in higher admission rates for respiratory and cardiovascular diseases. This builds on existing evidence highlighting the complex relationships between health and housing. While energy efficiency measures can improve health outcomes (especially when targeting those with chronic respiratory illness), reduced household ventilation rates can impact indoor air quality for example and increase the risk of diseases such as asthma. Alternatively, these findings could be due to the ecological study design, reverse causality, or the non-detection of more vulnerable subpopulations, as well as the targeting of areas with poor housing stock, low income households, and the lack of "whole house approaches" when retrofitting the existing housing stock. CONCLUSION: To be sustainable, household energy efficiency policies and resulting interventions must account for whole house approaches (i.e. consideration of the whole house and occupant lifestyles). These must consider more alternative 'greener' and more sustainable measures, which are capable of accounting for variable lifestyles, as well as the need for adequate heating and ventilation. Larger natural experiments and more complex modelling are needed to further investigate the impact of ongoing dramatic changes in the housing stock and health. STUDY IMPLICATIONS: This study supports the need for more holistic approaches to delivering healthier indoor environments, which must consider a dynamic and complex system with multiple interactions between a range of interrelated factors. These need to consider the drivers and pressures (e.g. quality of the built environment and resident behaviours) resulting in environmental exposures and adverse health outcomes.


Assuntos
Poluição do Ar em Ambientes Fechados , Exposição Ambiental , Hospitalização , Habitação , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Poluição do Ar em Ambientes Fechados/análise , Asma/etiologia , Estudos Transversais , Inglaterra , Exposição Ambiental/análise , Feminino , Calefação , Hospitalização/estatística & dados numéricos , Humanos , Masculino , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/etiologia , Ventilação , Adulto Jovem
8.
Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi ; 31(3): 285-290, 2019 Jul 26.
Artigo em Chinês | MEDLINE | ID: mdl-31544408

RESUMO

OBJECTIVE: To investigate the pathogenicity of Pneumocystis and its association with the development of chronic obstructive pulmonary disease (COPD). METHODS: The rat model of Pneumocystis pneumonia (PCP) was induced by intraperitoneal injection with dexamethasone, which was confirmed by pathogenic detection. The pathologic changes of rat lung specimens were examined using conventional HE staining, and the expression of inflammatory cells were detected by flow cytometry in bron-choalveolar lavage fluid (BALF) and splenic tissues of the rat model of PCP. In addition, the serum levels of matrix metalloproteinase 8 (MMP-8) and MMP-9 were measured using enzyme-linked immunosorbent assay (ELISA). RESULTS: Fusion and atrophy of alveolar spaces and hyperplasia of lung tissue were seen in the lung specimens of the rat model of PCP, and foam-like alveolar exudates and infiltration of inflammation cells were observed in the alveolar space, while severe infections exhibited consolidation of lung, which was similar to pathological features of COPD. The counts of CD8+ T lymphocytes (t = -7.920 and -12.514, P < 0.01), macrophages (t = -7.651 and -14.590, P < 0.01) and granulocytes (t = -10.310 and -16.578, P < 0.01) significantly increased and the counts of CD4+ T lymphocytes (t = 6.427 and 18.579, P < 0.01) significantly reduced in the BALF and splenic specimens of the rats with PCP relative to those without PCP. In addition, higher serum MMP-8 (t = -8.689, P < 0.01) and MMP-9 levels (t = -7.041, P < 0.01) were measured in rats with PCP than in those without PCP. CONCLUSIONS: Pneumocystis infection may be associated with the development and progression of COPD.


Assuntos
Pneumocystis , Pneumonia por Pneumocystis , Doença Pulmonar Obstrutiva Crônica/etiologia , Animais , Líquido da Lavagem Broncoalveolar/microbiologia , Modelos Animais de Doenças , Pulmão/microbiologia , Pneumocystis/patogenicidade , Pneumonia por Pneumocystis/complicações , Pneumonia por Pneumocystis/microbiologia , Doença Pulmonar Obstrutiva Crônica/microbiologia , Ratos , Virulência
10.
Toxicol Lett ; 316: 10-19, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31476341

RESUMO

Rapid risk assessment models for different types of cigarette smoke extract (CSE) exposure are critical to understanding the etiology of chronic obstructive pulmonary disease. The present study investigated inflammation of cultured tracheal tissues with CSE exposure. Rat trachea rings were isolated, cultured, then exposed to various concentrations of CSE from 3R4 F reference cigarettes for 4 h. Tissue/cellular morphology, ultrastructure, viability and damage, inflammatory cell infiltration, and inflammatory protein levels were measured and compared to untreated controls. Human bronchial epithelial cells (BEAS-2B) exposed to 0 or 300 µg/mL CSE were cocultured with macrophages to assess extent of mobilization and phagocytosis. Endotracheal epithelium cilia densities were significantly reduced with increasing CSE concentrations, while mucous membranes became increasingly disordered; both eventually disappeared. Macrophages became larger as the CSE concentration increased, with microvilli and extended pseudopodium covering their surface, and many primary and secondary lysosomes present in the cytoplasm. Inflammatory cell infiltration also increased with increasing CSE dose, as did intracellular adhesion molecule-1(ICAM-1), interleukin-6(IL-6). The method described here may be useful to qualitatively characterized the effects of the compound under study. Then, we use BEAS-2B cell line system to strength the observation made in the cultured tissues. Probably, an approach to integrate results from both experiments will facilitate its application. These results demonstrate that cultured rat tracheal rings have a whole-tissue structure that undergoes inflammatory processes similar to in vivo tissues upon CSE exposure.


Assuntos
Células Epiteliais/efeitos dos fármacos , Macrófagos/efeitos dos fármacos , Doença Pulmonar Obstrutiva Crônica/etiologia , Fumaça/efeitos adversos , Fumar/efeitos adversos , Tabaco/efeitos adversos , Traqueia/efeitos dos fármacos , Animais , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Técnicas de Cocultura , Células Epiteliais/metabolismo , Células Epiteliais/ultraestrutura , Humanos , Mediadores da Inflamação/metabolismo , Molécula 1 de Adesão Intercelular/metabolismo , Interleucina-6/metabolismo , Macrófagos/metabolismo , Macrófagos/ultraestrutura , Masculino , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/patologia , Ratos Sprague-Dawley , Medição de Risco , Fatores de Tempo , Técnicas de Cultura de Tecidos , Traqueia/metabolismo , Traqueia/ultraestrutura
11.
Pol Merkur Lekarski ; 47(278): 70-71, 2019 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-31473756

RESUMO

Although alpha-1 antitrypsin (A1AT) deficiency represents one of the most common genetically conditioned diseases in the population of Caucasian adult individuals, it is rarely diagnosed. Alpha-1 antitrypsin is an important component of the anti-proteolytic protection in the lungs. Individuals affected by the protein deficiency are exposed to a higher risk of developing chronic obstructive pulmonary disease (COPD), emphysema or liver diseases. A CASE REPORT: A 52-year-old farmer, non-smoker, spraying orchards since the age of 15 years, was admitted to the Department with dyspnea at rest and productive cough. He had a medical history of COPD, congestive heart failure, generalized emphysema of ten years' duration On admission the patient's general condition was satisfactory (fair). Physical examination showed symmetric expiratory wheezing over the upper and lower fields of the lungs with loss of vesicular murmur in the lower fields. Spirometry revealed a severe chronic bronchial obstruction, and an arterial blood gas test showed hypoxemia. Laboratory tests demonstrated an increased concentration of inflammatory markers. High resolution computed tomography (HRCT) of the chest showed evidence of generalized emphysema, bronchiectasis and exacerbation of peribronchial inflammatory changes. Intensive anti-inflammatory, bronchodilator treatment and antibiotic therapy were implemented, which resulted in an optimal improvement of the patient's condition. Based on the whole clinical picture A1AT deficiency was suspected. Alpha-1-antitrypsin deficiency, MZ phenotype, with 65 mg/dl concentration was diagnosed. CONCLUSIONS: Diagnostic tests for alpha-1 antitrypsin deficiency should always be considered in patients with emphysema or symptomatic COPD identified at an early age. In the described case the period between occurrence of clinical signs and establishing the diagnosis was ten years, which proves that there is a strong need to spread knowledge on A1AT among medical professionals. Otherwise, most of the patients will lose their chance of modifying their lifestyle or receiving proper treatment that could prevent the progression of changes in the lungs.


Assuntos
Doença Pulmonar Obstrutiva Crônica , Enfisema Pulmonar , Deficiência de alfa 1-Antitripsina , Adulto , Fazendeiros , Humanos , Masculino , não Fumantes , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/etiologia , Enfisema Pulmonar/diagnóstico , Enfisema Pulmonar/etiologia , Deficiência de alfa 1-Antitripsina/complicações , Deficiência de alfa 1-Antitripsina/diagnóstico
12.
Nutrients ; 11(9)2019 Aug 29.
Artigo em Inglês | MEDLINE | ID: mdl-31470503

RESUMO

Chronic obstructive pulmonary disease (COPD), a lung disease caused by chronic exposure to cigarette smoke, increases the number of inflammatory cells such as macrophages and neutrophils and emphysema. Isoflavone is a polyphenolic compound that exists in soybeans. Daidzein and genistein, two types of isoflavones, have been reported to have anti-inflammatory effects in various organs. We hypothesized that the daidzein-rich soy isoflavone aglycones (DRIAs) attenuate cigarette smoke-induced emphysema in mice. Mice were divided into four groups: the (i) control group, (ii) isoflavone group, (iii) smoking group, and (iv) isoflavone + smoking group. The number of inflammatory cells in the bronchoalveolar lavage fluid (BALF) and the airspace enlargement using the mean linear intercept (MLI) were determined 12 weeks after smoking exposure. Expressions of neutrophilic inflammatory cytokines and chemokines were also examined. In the isoflavone + smoking group, the number of neutrophils in BALF and MLI was significantly less than that in the smoking group. Furthermore, the gene-expressions of TNF-α and CXCL2 (MIP-2) in the isoflavone + smoking group were significantly less than those in the smoking group. Supplementation of the COPD murine model with DRIAs significantly attenuates pathological changes of COPD via suppression of neutrophilic inflammation.


Assuntos
Anti-Inflamatórios/farmacologia , Isoflavonas/farmacologia , Pulmão/efeitos dos fármacos , Infiltração de Neutrófilos/efeitos dos fármacos , Neutrófilos/efeitos dos fármacos , Pneumonia/tratamento farmacológico , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Enfisema Pulmonar/tratamento farmacológico , Fumaça , Produtos do Tabaco , beta-Glucanas/farmacologia , Animais , Citocinas/imunologia , Citocinas/metabolismo , Modelos Animais de Doenças , Mediadores da Inflamação/imunologia , Mediadores da Inflamação/metabolismo , Pulmão/imunologia , Pulmão/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Neutrófilos/imunologia , Neutrófilos/metabolismo , Pneumonia/etiologia , Pneumonia/imunologia , Pneumonia/metabolismo , Doença Pulmonar Obstrutiva Crônica/etiologia , Doença Pulmonar Obstrutiva Crônica/imunologia , Doença Pulmonar Obstrutiva Crônica/metabolismo , Enfisema Pulmonar/etiologia , Enfisema Pulmonar/imunologia , Enfisema Pulmonar/metabolismo , Transdução de Sinais
13.
Medicina (Kaunas) ; 55(9)2019 Sep 10.
Artigo em Inglês | MEDLINE | ID: mdl-31510089

RESUMO

Background and Objectives: The current study was performed to evaluate the prevalence of periodontitis and to examine the association between reduced pulmonary function and periodontitis using Sixth Korea National Health and Nutrition Examination Survey (KNHANES) in 2014. Materials and Methods: A cross-sectional evaluation was conducted to estimate the prevalence of periodontitis and to examine the association between periodontitis and reduced pulmonary function while adjusting for sociodemographic characteristics and current smoking status in survey participants between 40 and 79 years old. The presence of periodontitis was evaluated by community periodontal index defined by the World Health Organization, and the assessments of reduced pulmonary function data were made as "normal," "restrictive impairment," or "obstructive impairment." Results: A total of 4004 survey participants representing 25.4 million Koreans were included in the study. Overall, 41.1% of the study population were determined to have periodontitis, and 22.1% had reduced pulmonary function; 7.9% and 14.2% had restrictive- and obstructive- pulmonary impairments, respectively. Age, male gender, and current smoking status were positive predictors for periodontitis. Insurance coverage by workplace and higher education were protective factors against periodontitis. The association between periodontitis and restrictive impairment (adjusted odds ratio (OR) = 1.059, 95% CI 0.729-1.540) or obstructive impairment (adjusted OR = 1.140, 95% CI 0.849-1.530) was not significant. Conclusions: For Koreans, 40-79 years old, age, smoking status, gender, education, and insurance coverage were significant predictors of periodontitis. The prevalence of periodontitis was not significantly associated with reduced pulmonary function. To better understand the relationship between periodontitis and reduced pulmonary function, well-designed and larger scale epidemiologic studies are needed.


Assuntos
Pneumopatias/etiologia , Periodontite/epidemiologia , Adulto , Idoso , Estudos Transversais , Feminino , Humanos , Pneumopatias/epidemiologia , Masculino , Pessoa de Meia-Idade , Inquéritos Nutricionais , Índice Periodontal , Periodontite/complicações , Prevalência , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , República da Coreia/epidemiologia , Fatores de Risco , Fumar/epidemiologia
14.
Int J Chron Obstruct Pulmon Dis ; 14: 1527-1537, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31371938

RESUMO

Purpose: Cigarette smoke produces a high level of acrolein, which is thought to be pathogenically involved in the development of chronic obstructive pulmonary disease (COPD). The present study investigated the pathological role of acrolein in the development of COPD. Patients and methods: Acrolein concentration was measured in plasmas obtained from 47 patients with COPD and 18 current smokers without COPD, and in supernatants of homogenized lung tissues obtained from 10 never-smokers, 8 current smokers, and 8 patients with COPD by high-performance liquid chromatography. Oxidant status and antioxidant activity were measured using derivatives of reactive oxygen metabolite (d-ROM) and bio-antioxidant power (BAP), respectively, in the Free Radical Elective Evaluation FRAS4 system. In addition, immunohistochemistry was used to evaluate the over-presentation of acrolein in lung tissues of patients with COPD. Results: Plasma concentrations of acrolein were significantly higher in the patients with COPD than the non-COPD smokers (P<0.001), which significantly correlated with the oxidant status in patients with COPD (R=0.69, P<0.05). Similar pathological alterations in acrolein concentrations were found in the lung tissue supernatants of patients with COPD, which significantly correlated with the oxidant status in patients with COPD. Furthermore, acrolein was strongly expressed in the lung tissues of patients with COPD. Conclusion: The increased acrolein concentrations were highly involved in the pathogenesis of COPD through interference in the balance of oxidative stress versus antioxidant potentiality.


Assuntos
Acroleína/sangue , Pulmão/metabolismo , Estresse Oxidativo , Doença Pulmonar Obstrutiva Crônica/sangue , Fumar/efeitos adversos , Idoso , Biomarcadores/sangue , Estudos de Casos e Controles , Feminino , Humanos , Masculino , não Fumantes , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/etiologia , Fumantes , Fumar/sangue
15.
Environ Sci Pollut Res Int ; 26(30): 31225-31233, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31463744

RESUMO

Few researches have been investigated on the effects of ambient air pollutants from coal combustion on acute exacerbation of chronic obstructive pulmonary disease (AECOPD) hospitalizations. The whole time series was split into heating season and non-heating season. We used a quasi-Poisson generalized linear regression model combined with distributed lag non-linear models (DLNMs) to estimate the relative cumulative risk and calculate the air pollutant hospitalization burden of AECOPD for lag 0-7 days in heating season and non-heating season. There were higher PM2.5, PM10, NO2, SO2, and CO concentrations in heating seasons than non-heating season in Shijiazhuang; however, O3 was higher in non-heating season than heating season. The AECOPD-associated relative cumulative risks for PM2.5, PM10, NO2, and SO2 for lag 0-7 days were significantly positively associated with hospitalization in heating and non-heating season; we found that the cumulative relative risk of NO2 was the greatest in every 1 unit of air pollutants during the heating season and the cumulative relative risk of SO2 was the greatest during the non-heating season. The results showed that 17.8%, 12.9%, 1.7%, 16.7%, and 10.5% of AECOPD hospitalizations could be attributable to PM2.5, PM10, SO2, NO2, and CO exposure in heating season, respectively. However, the results showed that 19.5%, 22.4%, 15%, 8.3%, and 10.4% of AECOPD hospitalizations could be attributable to PM2.5, PM10, SO2, NO2, and O3 exposure in non-heating season, respectively. The attributable burden of AECOPD hospitalization in heating season and non-heating season are different. PM2.5, PM10, NO2, and CO are the main factors of heating season, while PM10, PM2.5, SO2, and O3 are the main factors of non-heating season. In conclusions, the centralized heating can change the influence of attributable risk. When government departments formulate interventions to reduce the risk of acute hospitalization of chronic obstructive pulmonary disease (COPD), the influence of heating on disease burden should be considered.


Assuntos
Poluição do Ar/análise , Hospitalização/estatística & dados numéricos , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , China/epidemiologia , Calefação , Humanos , Doença Pulmonar Obstrutiva Crônica/etiologia , Fatores de Risco , Estações do Ano
16.
Environ Sci Pollut Res Int ; 26(30): 30866-30875, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31446603

RESUMO

Few studies have investigated the acute exacerbations of chronic obstructive pulmonary disease (AECOPD)-associated attributable burden under exposure to high levels of air pollution among Asians. Data on hospitalization for AECOPD, air pollution and meteorological factors from 1 January 2013 to 31 December 2016 were collected in Shijiazhuang, China. We used a Poisson generalized linear regression model combined with a distributed lag nonlinear model (DLNM) to evaluate the relative cumulative risk for a lag of 0-7 days and examined the potential effect modifications by age and sex via stratification analyses, controlling for long-term trends, seasonal patterns, meteorological factors, and other possible confounders. Then, we computed hospitalization percentages attributable to air pollutants. The AECOPD-associated relative cumulative risks for PM2.5, PM10, NO2, SO2, and CO for a lag of 0-7 days were significantly positively correlated with hospitalization. The associations were stronger in females and retired patients. The NO2 Cum RR of AECOPD admission was the greatest. A 10µg/m3 increase in daily NO2 concentration was associated with 6.7% and 5.7% increases in COPD hospitalizations in the retired and female groups, respectively. The results showed that 13%, 9.4%, 1.7%, 9.7%, and 8.8% of AECOPD hospitalizations were attributable to exposure to PM2.5, PM10, SO2, NO2, and CO, respectively. If the air pollutant concentration was reduced to the 24-h average grade II levels of NAAQS of China, the AECOPD attributable percentage for PM2.5 and PM10 would decrease by 80%. The air pollutants PM2.5, PM10, SO2, NO2, and CO were significantly relevant to AECOPD-associated hospitalization. The associations differed by individual characteristics. The retired and female populations were highly vulnerable.


Assuntos
Poluição do Ar/efeitos adversos , Hospitalização/estatística & dados numéricos , Material Particulado/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Idoso , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/análise , China/epidemiologia , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Masculino , Conceitos Meteorológicos , Pessoa de Meia-Idade , Material Particulado/análise
17.
J Bras Pneumol ; 45(3): e20180314, 2019 Jun 27.
Artigo em Inglês, Português | MEDLINE | ID: mdl-31271604

RESUMO

Smoking is the leading cause of respiratory disease (RD). The harmful effects of smoking on the respiratory system begin in utero and influence immune responses throughout childhood and adult life. In comparison with "healthy" smokers, smokers with RD have peculiarities that can impede smoking cessation, such as a higher level of nicotine dependence; nicotine withdrawal; higher levels of exhaled carbon monoxide; low motivation and low self-efficacy; greater concern about weight gain; and a high prevalence of anxiety and depression. In addition, they require more intensive, prolonged treatment. It is always necessary to educate such individuals about the fact that quitting smoking is the only measure that will reduce the progression of RD and improve their quality of life, regardless of the duration and severity of the disease. Physicians should always offer smoking cessation treatment. Outpatient or inpatient smoking cessation treatment should be multidisciplinary, based on behavioral interventions and pharmacotherapy. It will thus be more effective and cost-effective, doubling the chances of success.


Assuntos
Doenças Respiratórias/etiologia , Doenças Respiratórias/terapia , Abandono do Hábito de Fumar , Fumar/efeitos adversos , Tabagismo/complicações , Humanos , Neoplasias Pulmonares/etiologia , Neoplasias Pulmonares/terapia , Doença Pulmonar Obstrutiva Crônica/etiologia , Doença Pulmonar Obstrutiva Crônica/terapia , Fatores de Risco , Tabagismo/terapia , Tuberculose Pulmonar/etiologia , Tuberculose Pulmonar/terapia
18.
Biomed Res Int ; 2019: 2025636, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31341890

RESUMO

Chronic obstructive pulmonary disease (COPD) and lung cancer, closely related to smoking, are major lung diseases affecting millions of individuals worldwide. The generated gas mixture of smoking is proved to contain about 4,500 components such as carbon monoxide, nicotine, oxidants, fine particulate matter, and aldehydes. These components were considered to be the principle factor driving the pathogenesis and progression of pulmonary disease. A large proportion of lung cancer patients showed a history of COPD, which demonstrated that there might be a close relationship between COPD and lung cancer. In the early stages of smoking, lung barrier provoked protective response and DNA repair are likely to suppress these changes to a certain extent. In the presence of long-term smoking exposure, these mechanisms seem to be malfunctioned and lead to disease progression. The infiltration of inflammatory cells to mucosa, submucosa, and glandular tissue caused by inhaled cigarette smoke is responsible for the destruction of matrix, blood supply shortage, and epithelial cell death. Conversely, cancer cells have the capacity to modulate the proliferation of epithelial cells and produce of new vascular networks. Comprehension understanding of mechanisms responsible for both pathologies is necessary for the prevention and treatment of COPD and lung cancer. In this review, we will summarize related articles and give a glance of possible mechanism between cigarette smoking induced COPD and lung cancer.


Assuntos
Remodelação das Vias Aéreas , Barreira Alveolocapilar , Fumar Cigarros , Matriz Extracelular , Neoplasias Pulmonares , Doença Pulmonar Obstrutiva Crônica , Barreira Alveolocapilar/metabolismo , Barreira Alveolocapilar/patologia , Fumar Cigarros/efeitos adversos , Fumar Cigarros/metabolismo , Fumar Cigarros/patologia , Matriz Extracelular/metabolismo , Matriz Extracelular/patologia , Humanos , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/patologia , Fatores de Tempo
20.
Zhonghua Liu Xing Bing Xue Za Zhi ; 40(6): 686-691, 2019 Jun 10.
Artigo em Chinês | MEDLINE | ID: mdl-31238620

RESUMO

Objective: To explore the short-term effects of ambient PM(2.5) on the outpatient visits of chronic obstructive pulmonary disease (COPD) in Ningbo city. Methods: Through the regional health information platform, number of daily COPD outpatients from the four general hospitals in Ningbo was gathered. Related data on meteorological and air pollution from 2014 to 2016 was also collected. Generalized additive model (GAM) of Possion regression was used to estimate the impact of PM(2.5) pollution on COPD outpatients and the lagging effects. Results: In cold (November- April) or warm seasons (May-October), an 10 µg/m(3) increase of PM(2.5) would result in the excessive number of COPD outpatients as 1.87% (95%CI: 0.98%-2.76%), 2.09% (95%CI: 1.11%-3.08%) and 2.56% (95%CI: 0.56%-4.59%), respectively. In terms of the short-term effects of PM(2.5) the strongest was seen in the days of warm season but without delay (P<0.05). The strongest effect appeared at day 4 in cold season and the effect was particularly significant seen in the over 65 year-old group or in the female population. After the introduction of PM(10), SO(2) and NO(2), the concentration of PM(2.5), did not show significant effect on the number of hospital visits due to COPD on the same day (P>0.05). The effect of COPD on the fourth day showed a slight change after the lagging, and the effect was statistically significant (P<0.05). Conclusion: The increase of PM(2.5) concentration in Ningbo was related to the increase of COPD outpatient numbers. Effective prevention measures should be taken to protect the vulnerable population and to reduce the risk of COPD.


Assuntos
Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Ambulatório Hospitalar/estatística & dados numéricos , Pacientes Ambulatoriais/estatística & dados numéricos , Material Particulado/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/etiologia , Idoso , Poluição do Ar/estatística & dados numéricos , Assistência Ambulatorial , Exposição Ambiental/estatística & dados numéricos , Feminino , Humanos , Material Particulado/análise , Doença Pulmonar Obstrutiva Crônica/epidemiologia , População Urbana
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