scholarly journals Association of NLRP1 Coding Polymorphism with Lung Function and Serum IL-1β Concentration in Patients Diagnosed with Chronic Obstructive Pulmonary Disease (COPD)

Genes ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 783 ◽  
Author(s):  
Ozretić ◽  
da Silva Filho ◽  
Catalano ◽  
Sokolović ◽  
Vukić-Dugac ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Minor Allele ◽  
Fine Tuning ◽  
Airflow Limitation ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Impact

Chronic obstructive pulmonary disease (COPD) is a chronic disease characterized by a progressive decline in lung function due to airflow limitation, mainly related to IL-1β-induced inflammation. We have hypothesized that single nucleotide polymorphisms (SNPs) in NLRP genes, coding for key regulators of IL-1β, are associated with pathogenesis and clinical phenotypes of COPD. We recruited 704 COPD individuals and 1238 healthy controls for this study. Twenty non-synonymous SNPs in 10 different NLRP genes were genotyped. Genetic associations were estimated using logistic regression, adjusting for age, gender, and smoking history. The impact of genotypes on patients’ overall survival was analyzed with the Kaplan–Meier method with the log-rank test. Serum IL-1β concentration was determined by high sensitivity assay and expression analysis was done by RT-PCR. Decreased lung function, measured by a forced expiratory volume in 1 s (FEV1% predicted), was significantly associated with the minor allele genotypes (AT + TT) of NLRP1 rs12150220 (p = 0.0002). The same rs12150220 genotypes exhibited a higher level of serum IL-1β compared to the AA genotype (p = 0.027) in COPD patients. NLRP8 rs306481 minor allele genotypes (AG + AA) were more common in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition of group A (p = 0.0083). Polymorphisms in NLRP1 (rs12150220; OR = 0.55, p = 0.03) and NLRP4 (rs12462372; OR = 0.36, p = 0.03) were only nominally associated with COPD risk. In conclusion, coding polymorphisms in NLRP1 rs12150220 show an association with COPD disease severity, indicating that the fine-tuning of the NLRP1 inflammasome could be important in maintaining lung tissue integrity and treating the chronic inflammation of airways.

LUNG FUNCTION IN SUBJECTS WITH OCCUPATIONAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE EXPOSED TO INDUSTRIAL AEROSOLS CONTAINING NANOPARTICLES

2021 ◽  
Author(s):  
L.A. Shpagina ◽  
◽  
E.B. Logashenko ◽  
E.V. Anikina ◽  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Silica Nanoparticles ◽  
Pulmonary Disease ◽  
Mass Concentration ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Volumes ◽  
Obstructive Pulmonary Disease ◽  
Occupational Copd

Abstract: Despite decrease in industrial aerosol impact on workers’ health there are disproportionately high prevalence of occupational lung diseases. So, it is of interest to investigate the role of nanoparticles. Objective was to establish lung function features in subjects with occupational chronic obstructive pulmonary disease (COPD) exposed to aerosols containing nanoparticles. Methods. It was a cross-sectional observational study. Subjects with occupational COPD (GOLD 2011-2021 criteria) exposed to aerosols containing metal (n=26) or silica nanoparticles (n=24) enrolled. Comparison group – tobacco smokers with COPD (n=50). Nanoparticles at workplaces air were measured by inductively coupled plasma atomic emission spectrometry and by scanning electron microscopy. Groups were matched by gender, age, COPD duration. Results. Occupational COPD in conditions of metal nanoparticles exposure was characterized by severe airflow limitation – forced expiratory volume in one second (FEV1) was 38%(35%;42%), by prominent increase in lung volumes – functional residual capacity (FRC) was 192% (184%;203%) and by highest decrease in diffusing lung capacity for carbon monoxide (DLco/Va), 34% (31%;38%). In occupational COPD subjects exposed to silica nanoparticles mild airflow limitation, mild increase in lung volumes and substantial decrease in DLco/Va, were seen. In logistic regression model metal nanoparticles mass concentration was associated with DLco/Va, FRC, FEV1, Raw and silica nanoparticles mass concentration – with DLco and FEV1. Conclusion. Nanoparticles in industrial aerosols are associated with occupational COPD phenotype.

scholarly journals Role of Diet in Chronic Obstructive Pulmonary Disease Prevention and Treatment

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1357 ◽  
Author(s):  
Egeria Scoditti ◽  
Marika Massaro ◽  
Sergio Garbarino ◽  
Domenico Maurizio Toraldo
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Dietary Patterns ◽  
Scientific Evidence ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Obstructive Pulmonary Disease ◽  
Prevention And Treatment ◽  
The Impact

Chronic obstructive pulmonary disease is one of the leading causes of morbidity and mortality worldwide and a growing healthcare problem. Identification of modifiable risk factors for prevention and treatment of COPD is urgent, and the scientific community has begun to pay close attention to diet as an integral part of COPD management, from prevention to treatment. This review summarizes the evidence from observational and clinical studies regarding the impact of nutrients and dietary patterns on lung function and COPD development, progression, and outcomes, with highlights on potential mechanisms of action. Several dietary options can be considered in terms of COPD prevention and/or progression. Although definitive data are lacking, the available scientific evidence indicates that some foods and nutrients, especially those nutraceuticals endowed with antioxidant and anti-inflammatory properties and when consumed in combinations in the form of balanced dietary patterns, are associated with better pulmonary function, less lung function decline, and reduced risk of COPD. Knowledge of dietary influences on COPD may provide health professionals with an evidence-based lifestyle approach to better counsel patients toward improved pulmonary health.

scholarly journals INTERACTION BETWEEN CLINICAL AND PSYCHOLOGICAL CHANGES AMONG PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND PULMONARY TUBERCULOSIS CO-MORBIDITY

2019 ◽  
Vol 72 (4) ◽  
pp. 635-638
Author(s):  
Natalia V. Zhovanyk ◽  
Mariana I. Tovt-Korshynska
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Tuberculosis ◽  
Pulmonary Disease ◽  
Airflow Limitation ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Co Morbidity ◽  
Situational Anxiety ◽  
Personal Anxiety

Introduction: The association of chronic obstructive pulmonary disease and pulmonary tuberculosis is an important medical and social problem with a significant burden in terms of morbidity and mortality. The course and prognosis of chronic diseases such as chronic obstructive pulmonary disease and pulmonary tuberculosis is greatly influenced not only by the clinical features but also by the psychological characteristics of the patient. The aim: To study the interaction between clinical changes and psychological characteristics considering gender differences among patients with chronic obstructive pulmonary disease in association with pulmonary tuberculosis. Materials and methods: We studied 41patients with chronic obstructive pulmonary disease (grade 2, 3, groups А, B, С, D) and infiltrative pulmonary tuberculosis co-morbidity (11 women and 30 men). All patients underwent general clinical examination, Acid-Fast Bacillus Testing, spirometry, Spielberg anxiety scale, Beck depression scale. Results: Patients with chronic obstructive pulmonary disease and pulmonary tuberculosis co-morbidity with more severe symptoms (according to Assesment Test scores) were older and, regardless of it, showed elevated depression and personal anxiety scores while situational anxiety scores were significantly lower compared to those with less severe symptoms. The correlation between symptoms severity and airflow limitation or smoking history was very mild. The elevated depression and personal anxiety could cause more severe symptoms. The revealed discrepancy between the symptoms severity and low levels of situational anxiety may be due to adaptation with displacement mechanisms to illness related chronic life stressors. We also observed elevated personal anxiety and depression scores together with less severe symptoms among female versus male chronic obstructive pulmonary disease/pulmonary tuberculosis patients, possibly reflecting physically ill women’s higher risk for depressive and anxiety related symptomatology relative to ill men. Conclusions: We revealed that among patients with chronic obstructive pulmonary disease and pulmonary tuberculosis co-morbidity symptoms severity was largely influenced by the patients’ age, gender and psychological factors (depression and personal anxiety), but, unexpectedly, much less – by airflow limitation and smoking history. We also found higher emotional distress, namely elevated personal anxiety and depression scores, in combination with less severe symptoms among female versus male patients with chronic obstructive pulmonary disease and pulmonary tuberculosis co-morbidity.

scholarly journals Adipokines NUCB2/Nesfatin-1 and Visfatin as Novel Inflammatory Factors in Chronic Obstructive Pulmonary Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Sirpa Leivo-Korpela ◽  
Lauri Lehtimäki ◽  
Mari Hämälainen ◽  
Katriina Vuolteenaho ◽  
Lea Kööbi ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Plasma Levels ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Diffusing Capacity ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Diffusing Capacity

COPD (chronic obstructive pulmonary disease) is a common lung disease characterized by airflow limitation and systemic inflammation. Recently, adipose tissue mediated inflammation has gathered increasing interest in the pathogenesis of the disease. In this study, we investigated the role of novel adipocytokines nesfatin-1 and visfatin in COPD by measuring if they are associated with the inflammatory activity, lung function, or symptoms. Plasma levels of NUCB2/nesfatin-1 and visfatin were measured together with IL-6, IL-8, TNF-α, and MMP-9, lung function, exhaled nitric oxide, and symptoms in 43 male patients with emphysematous COPD. The measurements were repeated in a subgroup of the patients after four weeks’ treatment with inhaled fluticasone. Both visfatin and NUCB2/nesfatin-1 correlated positively with plasma levels of IL-6 (r=0.341,P=0.027andrho=0.401,P=0.008, resp.) and TNF-α(r=0.305,P=0.052andrho=0.329,P=0.033, resp.) and NUCB2/nesfatin-1 also with IL-8 (rho=0.321,P=0.036) in patients with COPD. Further, the plasma levels of visfatin correlated negatively with pulmonary diffusing capacity (r=-0.369,P=0.016). Neither of the adipokines was affected by fluticasone treatment and they were not related to steroid-responsiveness. The present results introduce adipocytokines NUCB2/nesfatin-1 and visfatin as novel factors associated with systemic inflammation in COPD and suggest that visfatin may mediate impaired pulmonary diffusing capacity.

scholarly journals Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease and its correlation with disease severity

2017 ◽  
Vol 4 (2) ◽  
pp. 514 ◽  
Author(s):  
Vinod Singh Jatav ◽  
S. R. Meena ◽  
Shivcharan Jelia ◽  
Pankaj Jain ◽  
Devendra Ajmera ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Disease Severity ◽  
Airflow Limitation ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Female Ratio ◽  
Bedside Test ◽  
Duration Of Disease

Background: Chronic obstructive pulmonary disease is the fourth leading cause of mortality worldwide. It is defined as a disease state characterized by airflow limitation that is not fully reversible. Patients with chronic obstructive pulmonary disease (COPD) are at increased risk of cardiovascular disease. Electrocardiography (ECG) carries information about cardiac disease and prognosis in COPD patients. Present study was undertaken to correlate ECG changes with severity of COPD.Methods: 100 patients of COPD fulfilling the inclusion criteria coming to OPD/wards of NMCH, Kota were recruited. They were staged by pulmonary function test (PFT) and evaluated by electrocardiography. Statistical analysis of correlation was done with chi square test and statistical significance was taken p<0.05.Results: Mean age was 63.18±8.66 years, with male preponderance, male to female ratio 6.14:1. Mean duration of disease was 7.58±2.92 years, mean exposure to smoking of 25.06 pack years. Most common ECG finding was RAD which was present in 69% of cases, other ECG findings are P. pulmonale (45%), incomplete RBBB (15%), PPRW (35%), RVH (53%). All ECG findings except incomplete RBBB significantly correlated with disease severity (‘p’ value <0.05).Conclusions: COPD is more common in male in 5th to 7th decade of life, with a smoking history of more than 20 pack years. The occurrence of ECG findings increase as severity and duration of disease increase. It can be inferred that ECG is a useful bedside test to assess the severity of COPD.

scholarly journals Inhaled Steroids and Active Smoking Drive Chronic Obstructive Pulmonary Disease Symptoms and Biomarkers to a Greater Degree Than Airflow Limitation

2017 ◽  
Vol 12 ◽  
pp. 117727191773030
Author(s):  
Philip E Silkoff ◽  
Dave Singh ◽  
J Mark FitzGerald ◽  
Andreas Eich ◽  
Andrea Ludwig-Sengpiel ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Air Trapping ◽  
Obstructive Pulmonary Disease ◽  
Current Smoking ◽  
Clinical Biomarkers ◽  
Patient Reported ◽  
The Impact

Rationale: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease, and development of novel therapeutics requires an understanding of pathophysiologic phenotypes. Objectives: The purpose of the Airways Disease Endotyping for Personalized Therapeutics (ADEPT) study was to correlate clinical features and biomarkers with molecular characteristics in a well-profiled COPD cohort. Methods: A total of 67 COPD subjects (forced expiratory volume in the first second of expiration [FEV1]: 45%-80% predicted) and 63 healthy smoking and nonsmoking controls underwent multiple assessments including patient questionnaires, lung function, and clinical biomarkers including fractional exhaled nitric oxide (FENO), induced sputum, and blood. Measurements and main results: The impact of inhaled corticosteroids (ICSs), and to a lesser extent current smoking, was more associated with symptom control, exacerbation rates, and clinical biomarkers, than severity by FEV1. The ICS-treated smoking subjects were most symptomatic, with significantly elevated scores on patient-reported outcomes and more annual exacerbations ( P < .05). Inhaled corticosteroid users had greater airflow obstruction and air trapping compared with non-ICS users, regardless of smoking status. Smoking, regardless of ICS use, was associated with significantly lower FENO ( P < .05). Smoking, in non-ICS users, was associated with an elevated proportion of sputum neutrophils and reduced sputum macrophages. Increased serum C-reactive protein was observed in smokers but not in ICS and nonsmoking ICS users ( P < .05). In contrast, only air trapping and neutrophilic inflammation increased with severity, defined by postbronchodilator FEV1. Conclusions: Compared with COPD severity by FEV1, ICS use and current smoking were better determinants of clinical characteristics and biomarkers. Use of the ADEPT COPD data promises to prove useful in defining biological phenotypes to facilitate personalized therapeutic approaches.

scholarly journals Mild catalytic defects of tert rs61748181 polymorphism affect the clinical presentation of chronic obstructive pulmonary disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jialin Xu ◽  
Diego Madureira de Oliveira ◽  
Matthew A. Trudeau ◽  
Yang Yang ◽  
Jessica J. Y. Chin ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Longitudinal Study ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Clinical Presentation ◽  
Ex Vivo ◽  
Minor Allele ◽  
Rapid Decline ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

AbstractChronic obstructive pulmonary disease (COPD) is a disorder of accelerated lung aging. Multiple pieces of evidence support that the aging biomarker short telomeres, which can be caused by mutations in telomerase reverse transcriptase (TERT), contribute to COPD pathogenesis. We hypothesized that short telomere risk-associated single nucleotide polymorphisms (SNPs) in TERT, while not able to drive COPD development, nonetheless modify the disease presentation. We set out to test the SNP carrying status in a longitudinal study of smokers with COPD and found that rapid decline of FEV1 in lung function was associated with the minor allele of rs61748181 (adjusted odds ratio 2.49, p = 0.038). Biochemical evaluation of ex vivo engineered human cell models revealed that primary cells expressing the minor allele of rs61748181 had suboptimal telomere length maintenance due to reduced telomerase catalytic activity, despite having comparable cell growth kinetics as WT-TERT expressing cells. This ex vivo observation translated clinically in that shorter telomeres were found in minor allele carriers in a sub-population of COPD patients with non-declining lung function, over the 5-year period of the longitudinal study. Collectively, our data suggest that functional TERT SNPs with mild catalytic defects are nonetheless implicated in the clinical presentation of COPD.

A Review of the Advances in Chronic Obstructive Pulmonary Disease Treatment

2012 ◽  
Vol 25 (6) ◽  
pp. 576-582 ◽  
Author(s):  
Nicole L. Metzger ◽  
Lisa M. Lundquist
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Treatment Options ◽  
The United States ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Impact ◽  
New Evidence

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality across the globe and within the United States. Although several medication classes are used for COPD treatment, none of these medications have been shown to significantly improve long-term lung function or mitigate overall disease progression. This review describes the pharmacologic treatment options for COPD and highlights recent studies evaluating the impact of bronchodilators and combination therapy on lung function, mortality, quality of life, and exacerbations. Additionally, indacaterol and roflumilast, 2 new COPD treatment agents approved by the Food and Drug Administration in 2011, are discussed. Pharmacists play an important role in managing and educating patients with COPD and should utilize new evidence to make recommendations.

scholarly journals Epigenome-wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yung-Che Chen ◽  
◽  
Ying-Huang Tsai ◽  
Chin-Chou Wang ◽  
Shih-Feng Liu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Dna Methylations

AbstractWe hypothesized that epigenetics is a link between smoking/allergen exposures and the development of Asthma and chronic obstructive pulmonary disease (ACO). A total of 75 of 228 COPD patients were identified as ACO, which was independently associated with increased exacerbations. Microarray analysis identified 404 differentially methylated loci (DML) in ACO patients, and 6575 DML in those with rapid lung function decline in a discovery cohort. In the validation cohort, ACO patients had hypermethylated PDE9A (+ 30,088)/ZNF323 (− 296), and hypomethylated SEPT8 (− 47) genes as compared with either pure COPD patients or healthy non-smokers. Hypermethylated TIGIT (− 173) gene and hypomethylated CYSLTR1 (+ 348)/CCDC88C (+ 125,722)/ADORA2B (+ 1339) were associated with severe airflow limitation, while hypomethylated IFRD1 (− 515) gene with frequent exacerbation in all the COPD patients. Hypermethylated ZNF323 (− 296) / MPV17L (+ 194) and hypomethylated PTPRN2 (+ 10,000) genes were associated with rapid lung function decline. In vitro cigarette smoke extract and ovalbumin concurrent exposure resulted in specific DNA methylation changes of the MPV17L / ZNF323 genes, while 5-aza-2′-deoxycytidine treatment reversed promoter hypermethylation-mediated MPV17L under-expression accompanied with reduced apoptosis and decreased generation of reactive oxygen species. Aberrant DNA methylations may constitute a determinant for ACO, and provide a biomarker of airflow limitation, exacerbation, and lung function decline.

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