Chronic Obstructive Pulmonary Disease Smokers Research Articles

Lycopene Inhibits Smoke-Induced Chronic Obstructive Pulmonary Disease and Lung Carcinogenesis by Modulating Reverse Cholesterol Transport in Ferrets

Chronic obstructive pulmonary disease (COPD) and lung cancer share the same etiologic factor, cigarette smoking. Higher consumption of dietary lycopene has been associated with lower risks of COPD and lung cancer in smokers. We investigated whether lycopene feeding protects against COPD and lung cancer in ferrets, a nonrodent model that closely mimics cigarette smoke (CS)-induced chronic bronchitis, emphysema, and lung tumorigenesis in human. We also explored whether the protective effect of lycopene is associated with restoring reverse cholesterol transport (RCT), a key driver in persistent inflammation with CS exposure. Ferrets (4 groups, n = 12-16/group) were exposed to a combination of tobacco carcinogen (NNK) and CS with or without consuming lycopene at low and high doses (equivalent to ∼30 and ∼90 mg lycopene/day in human, respectively) for 22 weeks. Results showed that dietary lycopene at a high dose significantly inhibited NNK/CS-induced chronic bronchitis, emphysema, and preneoplastic lesions, including squamous metaplasia and atypical adenomatous hyperplasia, as compared with the NNK/CS alone (P < 0.05). Lycopene feeding also tended to decrease the lung neoplastic lesions. Furthermore, lycopene feeding significantly inhibited NNK/CS-induced accumulation of total cholesterol, and increased mRNA expression of critical genes related to the RCT (PPARα, LXRα, and ATP-binding cassette transporters ABCA1 and ABCG1) in the lungs, which were downregulated by the NNK/CS exposure. The present study has provided the first evidence linking a protective role of dietary lycopene against COPD and preneoplastic lesions to RCT-mediated cholesterol accumulation in lungs.

Overexpression of chitotriosidase and YKL-40 in peripheral blood and sputum of healthy smokers and patients with chronic obstructive pulmonary disease.

BackgroundDespite the absence of endogenous chitin in humans, chitinases are present in the serum of healthy subjects and their levels are increased in a variety of chronic inflammatory conditions. It has been shown that chitotriosidase and structurally related chitinase-like protein-YKL-40 contribute to the pathogenesis of COPD. However, details regarding the relation of their systemic and local airways levels remain unknown.ObjectivesTo examine peripheral blood and sputum chitotriosidase and YKL-40 expression in smokers and patients with COPD.MethodsForty patients with COPD, 20 healthy smokers and 10 healthy never-smokers were studied. Serum and induced sputum chitotriosidase protein and activity levels, YKL-40 concentrations, and their gene expression in sputum cells and peripheral blood mononuclear cells (PBMC) were evaluated.ResultsBoth chitotriosidase protein levels and activity were higher in sputum obtained from COPD subjects compared to healthy never-smokers (P<0.05 and P<0.01, respectively). A similar pattern was observed for PBMC chitotriosidase mRNA expression (P<0.001). YKL-40 serum concentrations were elevated in healthy smokers and COPD subjects compared to healthy never-smokers (P<0.001 and P<0.01, respectively). In sputum, YKL-40 levels were increased in COPD compared to healthy never-smokers (P<0.01). PBMC YKL-40 mRNA expression was increased in COPD and healthy smokers compared to healthy never-smokers (P<0.0001). No associations were found between chitotriosidase or YKL-40 peripheral blood levels and sputum levels.ConclusionsOur results demonstrate that chitotriosidase and YKL-40 are overexpressed in peripheral blood and airways in both healthy smokers and COPD subjects which may indicate smoking-related activation of macrophages, neutrophils, and epithelial cells.

Factors associated with chronic obstructive pulmonary disease exacerbation, based on big data analysis

Preventing exacerbation in chronic obstructive pulmonary disease (COPD) patients is crucial, but requires identification of the exacerbating factors. To date, no integrated analysis of patient-derived and external factors has been reported. To identify factors associated with COPD exacerbation, we collected data, including smoking status, lung function, and COPD assessment test scores, from 594 COPD patients in the Korean COPD subgroup study (KOCOSS), and merged these data with patients’ Korean Health Insurance Review and Assessment Service data for 2007–2012. We also collected primary weather variables, including levels of particulate matter <10 microns in diameter, daily minimum ambient temperature, as well as respiratory virus activities, and the logs of web queries on COPD-related issues. We then assessed the associations between these patient-derived and external factors and COPD exacerbations. Univariate analysis showed that patient factors, air pollution, various types of viruses, temperature, and the number of COPD-related web queries were associated with COPD exacerbation. Multivariate analysis revealed that the number of exacerbations in the preceding year, female sex, COPD grade, and influenza virus detection rate, and lowest temperature showed significant association with exacerbation. Our findings may help COPD patients predict when exacerbations are likely, and provide intervention as early as possible.

Chronic Obstructive Pulmonary Disease (COPD) Screening is Still a Challenge in Pakistan

Background: Chronic obstructive lung disease (COPD) is a highly preventable disease with smoking as most recognizable risk factor globally. COPD remains undiagnosed worldwide due to unavailability of gold standard spirometry. Technical difficulties in this procedure, faced by patient result in over and under diagnosis of this prevalent disease. Objective of this study was to screen the undiagnosed air way obstruction which reflects the COPD among the smokers and nonsmokers. PEFR was used for assessment, as it is simple, reliable and easily available way at most of the health care centers.&#x0D; Methodology: A cross sectional study was conducted from May 2018 to Dec 2018 at private medical institute and private hospital in Faisalabad. It comprised of 200 males (smokers and nonsmokers) who had no previous history of diagnosis of COPD. Relevant information related to smoking including pack years and medical history specially related to COPD was inquired on structured questionnaire. Air way obstruction was assessed by PEFR using vitalograph compact. Data was analyzed by SPSS 21 version. Continuous variables are presented as mean and standard deviation (SD) and compared by Independent t-test among study groups. Categorical variables are expressed as proportions and compared by X2 test. P value ? 0.05 was considered significant.&#x0D; Results: Results are showing that 91.56% of the studied smokers have air way obstruction based on yellow and red zones of PEFR. Out of total COPD smokers 62.7% were in yellow zone and 28.9% were in red zone. Only 29.1% of nonsmokers have PEFR values within yellow. None of nonsmoker was in red zone (P value 0.001*). PEFR was significantly lower in smokers in comparison to nonsmokers (P value 0.003*). 95.5% of Subjects in red zone were symptomatic, while only 51.2% of subjects in yellow zone were symptomatic considering mild to severe air flow obstruction.&#x0D; Conclusion: Smokers and nonsmokers have undiagnosed airway obstruction with symptoms reflecting COPD but greater proportion of smoker were involved. PEFR was lower in smokers as compared to nonsmokers.

Hypermethylation of mitochondrial transcription factor A induced by cigarette smoke is associated with chronic obstructive pulmonary disease

Purpose of the study: Cigarette smoking is a leading environmental contributor to chronic obstructive pulmonary disease (COPD), but its epigenetic regulation of mtTFA gene remains elusive. This study aims to explore the relationship of DNA methylation of mtTFA and cigarette smoking in COPD. Materials and Methods: We analyzed DNA methylation on mtTFA promoters in clinical samples from COPD patients and subjects with normal pulmonary function. Expression of mtTFA mRNA in the clinical samples and mtTFA mRNA and protein in human umbilical vein endothelial cells(HUVECs) treated with cigarette smoke extract (CSE) was evaluated. mtTFA mRNA and protein levels were measured to determine effects of demethylation agents on CSE-treated HUVECs. Results: The DNA methylation level of the mtTFA promoter was significantly increased in COPD group. Expression of mtTFA mRNA was downregulated in the lungs as a consequence of hypermethylation of mtTFA promoter. Expression of mtTFA mRNA and protein was downregulated in CSE-treated HUVECs as a consequence of hypermethylation of the mtTFA promoter. mtTFA expression in CSE-treated HUVECs was restored by the methylation inhibitor, 5-aza-2’-deoxycytidine(AZA). Conclusions: Cigarette smoke-induced hypermethylation of the mtTFA promoter is related to the initiation and progression of COPD. Our finding may provide a new strategy for the intervention of COPD by developing demethylation agents targeting mtTFA hypermethylation.

การศึกษาเบื้องต้นของผลการบอกอายุปอด (เพื่อสร้างแรงจูงใจ) ต่อการเลิกบุหรี่ในผู้ป่วย COPD

Objective: The aim of this research is to study the initial results of telling the lung age for motivation to quit smoking in COPD patients. Methods: Twenty-five smokers who diagnosed COPD more than 1 year and aged over 40 years old in COPD clinic, Siriraj Hospital, Thailand were recruited. They were informed the lung age (age of their lungs were calculated by spirometer) and advised to quit smoking after that enrolled the smoking cessation program. The outcome of quit smoke was measured repeated every 3, 6 and 12 months. Results: The stages of quitting smoking motivation in participants were 72% contemplation, 20% preparation and 8% pre-contemplation. Awareness about the lung age was the most motivation reason for quitting smoking (52%). The quit smoking rate was 16% in 3 and 6 months, and 25% in 12 months (total 24 subjects and 1 lost followed up). The reason of the participant that has successfully quit were 50% knowing the lung age. We founded that the subjects who good compliant will success in quit smoking. Conclusion: Telling the lung age in COPD smokers with a smoking cessation program can useful motivation tool for quit smoking. However, this is a pilot study so the future should be educated in more than a COPD patient group. Keywords: Smoking cessation; COPD; lung age

The Nocturnal Respiratory Rate in COPD Patients of Varying GOLD Severity with/without Nicotine Consumption: Calculation by Means of Breath Sound Analysis

Respiratory rate is an important risk marker and enables early detection of critically ill and vulnerable patients in clinical routine. The aim of this pilot study with 31 patients (COPD severity levels II - IV) was to determine the mean nocturnal respiratory rate based on breath sound recordings and to investigate the dependence of respiratory rate on COPD severity level and smoker status. The mean respiratory rate of the total collective was 19/min. For the COPD-GOLD severity levels, no significant differences in mean respiratory rate could be observed. When nicotine consumption is taken into account, active smokers showed a significantly higher mean respiratory rate of 20.84 ± 4.45/min compared to non-smokers with 17.41 ± 3.14/min (p < 0.05). In addition, active smokers in the study were significantly more frequent among patients with night-time wheezing (60 % vs. 23.8 %). This might suggest that smokers need to perform increased breathing work with increased breathing rate to compensate for oxygen deficiency in bronchial obstruction. The results of the present study show that with the acoustic recording of breath sounds, a reliable representation and calculation of the breath frequency is possible.

FGF Signaling in Lung Development and Disease: Human Versus Mouse.

Fibroblast growth factor 10 (FGF10) plays an important role in mouse lung development, injury, and repair. It is considered the main morphogen driving lung branching morphogenesis in rodents. While many studies have found FGF10 SNPs associated with COPD and branch variants in COPD smokers, there is no evidence of a causative role for FGF10 or these SNPs in human lung development and pediatric lung diseases. We and others have shown divergent roles for FGF10 in mouse lung development and early human lung development. Herein, we only review the existing literature on FGF signaling in human lung development and pediatric human lung diseases, comparing what is known in mouse lung to that in human lung.

Quantitative Assessment of Mucociliary Clearance in Smokers with Mild-to-Moderate Chronic Obstructive Pulmonary Disease and Chronic Bronchitis from Planar Radionuclide Imaging Using the Change in Penetration Index.

Background: Mucociliary clearance (MCC) rate from the lung has been shown to be reduced in chronic obstructive pulmonary disease (COPD). This study compared the use of change in penetration index (PI) with conventional whole lung clearance in assessing MCC in mild-to-moderate disease. Methods: Measurement of lung MCC using planar gamma camera imaging was performed in three groups: (1) healthy nonsmoking controls (n = 9), (2) smoking controls who were current smokers with normal lung function (n = 10), and (3) current smokers with mild-to-moderate COPD and bronchitis (n = 15). The mean (±standard deviation) forced expiratory volume at 1 second (FEV1) for the three groups was 109 (±18), 94 (±5), and 78 (±12), respectively. Following inhalation of a technetium-99m labeled aerosol, planar imaging was performed over 4 hours and then at 24 hours. Total lung clearance and tracheobronchial clearance (TBC; normalized to 24-hour clearance) were calculated. A novel parameter, the normalized change in PI (NOCHIP), was also evaluated. PI is the ratio of counts between outer and inner lung zones normalized to lung volume. Results: More aerosol was deposited in central airways in COPD compared to nonsmoking controls, using 24-hour clearance measurements (p < 0.001). Smoking controls had intermediate values. The optimal endpoint for MCC assessment was chosen to be 3 hours, when intersubject variability was minimal, while preserving a measure of early clearance. There was no statistical difference between the three groups in mean total lung clearance, or TBC, at 3 hours. NOCHIP at 3 hours was reduced significantly, compared to nonsmoking controls, in both smoking controls (p = 0.007) and COPD (p < 0.0001). It also correlated with FEV1 (p = 0.003). A higher proportion of smoking control subjects had NOCHIP values in the nonsmoking control range than in the COPD group. Conclusions: NOCHIP was a more sensitive measure of MCC than whole lung clearance and TBC in mild-to-moderate COPD.

Inflammatory mediators in exhaled breath condensate and peripheral blood of healthy donors and stable COPD patients

Objective: The aim of this work was to compare matrix metalloproteinase-9 and -12, tissue inhibitor of metalloproteinase-1 and -4, and neutrophil elastase in exhaled breath condensate (EBC) and peripheral blood of patients with COPD.Methods: Peripheral blood and EBC samples from COPD patients and healthy donors were collected. In serum and EBC, MMP-9, MMP-12, NE, TIMP-1, and TIMP-4 proteins were detected by ELISA. The mRNA expression levels of MMP-9, MMP-12, NE, TIMP-1, and TIMP-4 in peripheral blood mononuclear cells (PBMCs) were analyzed by qRT-PCR.Results: The protein levels of MMP-9 (p=.034) and MMP-12 (p=.041) in the EBC of COPD smokers were higher than those of COPD never-smokers. The concentrations of TIMP-1 (p=.072) and TIMP-4 (p=.084) in the EBC of COPD smokers were higher than those of COPD never-smokers; however, the difference was not statistically significant. MMP-9 (r=–0.78, p<.0001) and TIMP-1 (r=–0.71, p<.0001) levels in EBC were significantly negatively correlated with pulmonary function FEV1%pred. The protein levels of MMP-12 (r=–0.37, p=.034) and TIMP-4 (r=–0.34, p=.041) were also negatively correlated with FEV1%pred. The expression of MMP-9, MMP-12, NE, TIMP-1, and TIMP-4 in PBMCs and serum of COPD smokers were significantly higher than those of control never-smokers (p<.05).Conclusions: Exhaled MMP-9, MMP-12, TIMP-1, and TIMP-4 levels increased in stable COPD patients and were negatively correlated with FEV1%pred, which suggests the usefulness of their measurement in EBC for the monitoring of airway inflammation. However, to better assess their diagnostic or prognostic value, larger studies are necessary.

Association of HTR2A-1438G/A Genetic Polymorphism With Smoking and Chronic Obstructive Pulmonary Disease

IntroductionCigarette smoking is a major risk factor in the development of chronic obstructive pulmonary disease (COPD). Serotonin levels have been associated with COPD and smoking has been as a significant modulator. Elevated levels of serotonin are responsible for bronchoconstriction and pulmonary vasoconstriction and also nicotine dependence, thus serotonin response could be affected by genetic polymorphisms in transporters and receptors of serotonin. ObjectivesThe aim of the current study was to analyze the effect of SLC6A4 (5HTT_LPR) (rs25531) and HTR2A-1438G/A (rs6311) genetic polymorphisms on the relation between smoking habits and COPD. MethodsThe association between SLC6A4 (5HTT_LPR) (rs25531), HTR2A-1438G/A (rs6311), smoking degree and COPD was analyzed in a total of 77 COPD patients (active smokers) and 90 control subjects (active healthy smokers). The DNA was extracted of peripheral leukocytes samples and genotyping was performed using an allele specific polymerase chain reaction. ResultsThe distribution of SLC6A4 genotypes did not vary between healthy smokers and COPD patients (P=0.758). On the other hand, the A allele of HTR2A (rs6311) was significantly associated with COPD incidence in the trend model (P=0.02; 1.80 [1.04–3.11]). Among all smokers, this allele was also associated with the number of pack years smoked (P=0.02) and also, we observed a marginal association with FEV1/FVC values (P=0.06). ConclusionOur results point a possible role of the A allele of HTR2A (rs6311) in COPD pathogenesis, suggesting that this effect depends partly on tobacco consumption due to a gene-by-environment interaction.

Geographic Relationships Between Smoking and Chronic Lower Respiratory Disease in Delaware.

ObjectivesTo determine geographical relationships between smoking prevalence, COPD prevalence, and lower respiratory disease mortality in Delaware by census tract and county.MethodsData about Delaware residents with COPD, who are smokers, and/or have chronic lower respiratory diseases, respectively, were analyzed from publically accessible datasets posted on PolicyMap and Delaware Open Data. Data was linked to shapefiles in order to map prevalence and mortality rates by Delaware census tract and county. Geo-based descriptive analysis was conducted via choropleth maps.ResultsCOPD prevalence was higher in urban areas with high smoking prevalence. The highest proportion of census tracts with high COPD rates occurred in Sussex County and the lowest was in New Castle County. The highest crude and age-adjusted mortality rate due to chronic lower respiratory disease was in Sussex County and the lowest was in New Castle County. Chronic lower respiratory disease mortality was highest among white residents, increased as age increased, and occurred more frequently in females than in males.ConclusionSussex County had a high proportion of census tracts with high COPD rates and the highest mortality rate due to chronic lower respiratory disease. Urban census tracts displayed high rates of COPD prevalence and smoking prevalence. Identifying geographic focus areas can be used to direct future healthcare programs and public health initiatives. Future research should test statistical relationships between risk factors, geographic areas, and chronic lung disease outcomes.

An Ophthalmic Changes in Patients with Chronic Obstructive Pulmonary Disease: Case-Control Study

Purpose: To evaluate the prevalence of ophthalmological changes in patients with Chronic Obstructive Pulmonary Disease (COPD) cared for at the Pneumology and Ophthalmology Departments at Medical School Unifacisa-Campina Grande-Paraiba-Brazil.Materials and Methods: Twenty-two smoker patients with COPD (study group) and 22 healthy controls that underwent routine ophthalmological examination (control group) were enrolled in the investigation. They were homogeneous regarding age, gender, presence of Systemic Arterial Hypertension (SAH) and Diabetes Mellitus (DM). They were examined for the presence of cataract and Age Related Macular Disease (AMD).Results: The prevalence of ophthalmologic changes was significantly different in the two groups. Eight (36.4%)patients presented with cataract requiring surgical intervention, while one (4.5%) person in the control group had cataract (p = 0.0212). Regarding AMD, 10 (45.5%) smoker COPD patients had this disease, whereas in the control group, one (4.5%) person had this disease (p = 0.0039).Conclusion: From the results one can conclude that there is strong association between smokers diagnosed with COPD with cataract and AMD patients, reinforcing the need for a protocol for referral of these patients to the ophthalmologist.

Chronic Obstructive Pulmonary Disease in Latin America.

The PLATINO and PREPOCOL population-based studies documented the prevalence of chronic obstructive pulmonary disease (COPD) in several Latin American (Mexico City, Sao Paulo, Montevideo, Santiago and Caracas) and Colombian (Medellin, Bogota, Barranquilla, Bucaramanga and Cali) cities. COPD ranged between 6.2 and 19.6% in individuals ≥40 years of age, with substantial rates of underdiagnosis (up to 89%) but also overdiagnosis, mostly due to the lack of spirometric confirmation. The main risk factor was tobacco smoking, but male gender and age were also associated with COPD. COPD in never smokers represented about one third of the cases and was associated with previous history of tuberculosis or a diagnosis of asthma. COPD associated with biomass smoke exposure was a common clinical phenotype in Latin America, found as a risk factor in PREPOCOL and other observational studies in the region. Smoking has been decreasing in Latin America and efforts have been made to implement cleaner biomass stoves. Unfortunately, treatment of COPD in Latin America remains highly variable with low rates of smoking cessation counselling, low use of inhaled bronchodilators and influenza vaccination. A primary-care approach to COPD, particularly in the form of integrated programs is lacking but would be critical to improving rates of diagnosis and treatment of COPD.

The impact of cigarette smoke exposure, COPD, or asthma status on ABC transporter gene expression in human airway epithelial cells

ABC transporters are conserved in prokaryotes and eukaryotes, with humans expressing 48 transporters divided into 7 classes (ABCA, ABCB, ABCC, ABCD, ABDE, ABCF, and ABCG). Throughout the human body, ABC transporters regulate cAMP levels, chloride secretion, lipid transport, and anti-oxidant responses. We used a bioinformatic approach complemented with in vitro experimental methods for validation of the 48 known human ABC transporters in airway epithelial cells using bronchial epithelial cell gene expression datasets available in NCBI GEO from well-characterized patient populations of healthy subjects and individuals that smoke cigarettes, or have been diagnosed with COPD or asthma, with validation performed in Calu-3 airway epithelial cells. Gene expression data demonstrate that ABC transporters are variably expressed in epithelial cells from different airway generations, regulated by cigarette smoke exposure (ABCA13, ABCB6, ABCC1, and ABCC3), and differentially expressed in individuals with COPD and asthma (ABCA13, ABCC1, ABCC2, ABCC9). An in vitro cell culture model of cigarette smoke exposure was able to recapitulate select observed in situ changes. Our work highlights select ABC transporter candidates of interest and a relevant in vitro model that will enable a deeper understanding of the contribution of ABC transporters in the respiratory mucosa in lung health and disease.

Clinical, demographic and radiological profile of smoker COPD versus nonsmoker COPD patients at a tertiary care center in North India.

Introduction:Cigarette smoking is the most predominant risk factor for development of chronic obstructive pulmonary disease (COPD). However, a considerable amount of patients do develop COPD without exposure to cigarette smoking. We aimed to analyze the incidence, demographic and clinical profile of nonsmoker COPD subjects at a tertiary care center.Methods:In this prospective observational study, 410 patients were screened for dyspnea. On the basis of spirometry findings, 360 patients were diagnosed as COPD and enrolled into the study. Patients were categorized into 2 groups on the basis of smoking habits (smoker and nonsmoker COPD). Clinical and demographic attributes were compared in between these two groups. This study was conducted over a period of one year, from August 2014 to July 2015. All statistical analyses were performed using Statistical Package for the Social Sciences version 19.0 (SPSS Inc, Chicago, IL, USA). Values were considered to be statistically significant at P < 0.05.Results:Out of 360 COPD cases, about 2/3rd (60%) were smokers and the rest nonsmokers. Majority of the patients were in the age group of 51-70 years. The mean age of smokers with COPD was significantly higher than nonsmokers with COPD (59.29 ± 10.28 years vs. 53.90 ± 8.77 years; P = 0.0001). Overall, males were predominant (57.2%) but there were higher number of female patients in nonsmoker group (25% vs. 70%; P = 0.001). At presentation, majority of nonsmoker with COPD were in GOLD severity grade II while in the smoking cohort majority were in GOLD severity Grade III. Among the 144 nonsmoker COPD patients, the most important and statistically significant risk factor was exposure to biomass smoke (68.06%). Other risk factors were long-standing asthma (37.50%), lower respiratory tract infection in childhood (32.60%), exposure to outdoor air pollution (17.92%).Conclusion:Nonsmoker COPD is emerging as a distinctive phenotype. They have less impairment in airflow limitation, and a lower prevalence of emphysema, chronic cough, and sputum compared with their smoking counterparts.

The effect of cigarette smoking on the oxidant–antioxidant imbalance in patients with chronic obstructive pulmonary disease

Background Predisposing factors for chronic obstructive pulmonary disease (COPD) comprise endogenous genetic factors and exogenous factors such as positive and negative smoking, air pollution, inhalation of dust, and work-related chemicals. Because only a small percentage of smokers develop COPD, it is thought to arise as an outcome of environmental harm and a host’s response system, which boosts the tendency of the disease to arise. Objective To clarify the effect of smoking on the level of oxidant–antioxidant in patients with COPD. Patients and methods Thirty patients with COPD (20 smokers and 10 nonsmokers) and 40 healthy individuals (18 smokers and 22 nonsmokers) participated in this study. The investigations included measurement of malondialdehyde (MDA), superoxide dismutase (SOD) activity, catalase (CAT) activity, glutathione peroxidase (GPx), glutathione reductase (GR), vitamin C, and glutathione (GSH) content. Results SOD, CAT, GPx, GSH, GR, and vitamin C were significant lower (P Conclusion There is a significant reduction in the level of some antioxidants (SOD, GSH, and GPx) in smokers with COPD compared with nonsmokers with COPD, but other antioxidants (CAT, GR, and vitamin C) did not change significantly, whereas the oxidant levels (i.e., MDA) were relatively convergent in patients with COPD (smokers and nonsmokers). This, in turn, points to the modest role of smoking in the causation of oxidant–antioxidant imbalance in this disease.

Normal Routine Spirometry Can Mask Clinical and Physiologic Detection of COPD and Emphysema in Symptomatic Smokers

Normal Routine Spirometry Can Mask Clinical and Physiologic Detection of COPD and Emphysema in Symptomatic Smokers

Biomass smoke COPD has less tomographic abnormalities but worse hypoxemia compared with tobacco COPD.

Special attention has emerged towards biomass smoke-induced chronic obstructive pulmonary disease (COPD), providing new knowledge for prevention and therapeutic approach of non-smoker COPD patients. However, the understanding of biomass smoke COPD is still limited and somewhat controversial. The aim of the present study was to compare COPD exclusively caused by tobacco smoking with COPD exclusively caused by environmental or occupational exposures. For this cross-sectional study, COPD patients were recruited from outpatient clinics and formed two groups: non-smoker COPD group (n=16) with exposure to biomass smoke who did not smoke cigarette and tobacco smoker COPD group (n=15) with people who did not report biomass smoke exposure. Subjects underwent pulmonary function tests, thoracic high-resolution computed tomography, 6-min walk test, and sputum induction. The non-smoker COPD group had biomass smoke exposure of 133.3±86 hour-years. The tobacco COPD group smoked 48.5±27.4 pack-years. Women were 62.5 and 66.7%, respectively, of non-smokers and smokers. The non-smoker COPD group showed higher prevalence of dyspnea, lower arterial oxygen tension (PaO2), and lower arterial oxygen saturation (SaO2%) with similar spirometry results, lung volumes, and diffusion capacity. Regarding inflammatory biomarkers, differences were detected in sputum number of lymphomononuclear cells and in sputum concentrations of interleukin (IL)-6 and IL-8 with higher values in the smoker group. Emphysema was more prevalent in the tobacco smoker group, which also showed higher relative bronchial wall thickness and lower lung density by quantitative analysis. Biomass smoke induced more hypoxemia compared to tobacco in COPD patients with similar severity.

TRPC channels mediated calcium entry is required for proliferation of human airway smooth muscle cells induced by nicotine-nAChR

The present study was designed to explore the role of transient receptor potential canonical 3 (TRPC3) in nicotine-induced chronic obstructive pulmonary disease (COPD) and its underlying mechanism. In this study, the expression and localization of α5 nicotinic acetylcholine receptor (α5-nAchR) in lung tissues were determined by western blotting and immunohistochemistry. The quantitative real-time PCR (qRT-PCR) analysis was performed to examine the mRNA expression levels of α5-nAchR and TRPC3 in human airway smooth muscle cells (HASMCs). Cell viability was assessed by CCK-8 assay. Proliferation was detected by cell counting and EdU immunofluorescent staining. Fluorescence calcium imaging was carried out to measure cytosolic Ca2+ ([Ca2+]cyt) concentration. The results showed that the α5-nAchR and TRPC3 expressions were significantly up-regulated in lung tissues of COPD smokers. Nicotine promoted HASMC proliferation, which was accompanied by elevated α5-nAchR and TRPC3 expressions, basal [Ca2+]cyt, store-operated calcium entry (SOCE) and the rate of Mn2+ quenching in HASMCs. Further investigation indicated that nicotine-induced Ca2+ response and TRPC3 up-regulation was reversibly blocked by small interfering RNA (siRNA) suppression of α5-nAChR. The knockdown of TRPC3 blunted Ca2+ response and HASMC proliferation induced by nicotine. In conclusion, nicotine-induced HASMC proliferation was mediated by TRPC3-dependent calcium entry via α5-nAchR, which provided a potential target for treatment of COPD.