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.

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 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.

Smoking, Systemic Inflammation, and Airflow Limitation: A Mendelian Randomization Analysis of 98 085 Individuals From the General Population

2018 ◽  
Vol 21 (8) ◽  
pp. 1036-1044 ◽  
Author(s):  
Yunus Çolak ◽  
Shoaib Afzal ◽  
Peter Lange ◽  
Børge G Nordestgaard
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
General Population ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Tobacco Consumption ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
General Population Study ◽  
Former Smokers

Abstract Introduction Smoking is associated with systemic and local inflammation in the lungs. Furthermore, in chronic obstructive pulmonary disease, which is often caused by smoking, there is often systemic inflammation that is linked to lung function impairment. However, the causal pathways linking smoking, systemic inflammation, and airflow limitation are still unknown. We tested whether higher tobacco consumption is associated with higher systemic inflammation, observationally and genetically and whether genetically higher systemic inflammation is associated with airflow limitation. Methods We included 98 085 individuals aged 20–100 years from the Copenhagen General Population Study; 36589 were former smokers and 16172 were current smokers. CHRNA3 rs1051730 genotype was used as a proxy for higher tobacco consumption and the IL6R rs2228145 genotype was used for higher systemic inflammation. Airflow limitation was defined as forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) <70%. Results Difference in plasma level of C-reactive protein was 4.8% (95% CI = 4.4% to 5.2%) per 10 pack-year increase and 1.6% (95% CI = 0.4% to 2.8%) per T allele. Corresponding differences were 1.2% (95% CI = 1.1% to 1.3%) and 0.5% (95% CI = 0.3% to 0.8%) for fibrinogen, 1.2% (95% CI = 1.2% to 1.3%) and 0.7% (95% CI = 0.5% to 1.0%) for α1-antitrypsin, 2.0% (95% CI = 1.8% to 2.1%) and 0.7% (95% CI = 0.4% to 1.1%) for leukocytes, 1.9% (95% CI = 1.8% to 2.1%) and 0.8% (95% CI = 0.4% to 1.2%) for neutrophils, and 0.8% (95% CI = 0.7% to 1.0%) and 0.4% (95% CI = 0.1% to 0.7%) for thrombocytes. The differences in these levels were lower for former smokers compared with current smokers. The IL6R rs2228145 genotype was associated with higher plasma acute-phase reactants but not with airflow limitation. Compared with the C/C genotype, the odds ratio for airflow limitation was 0.95 (95% CI = 0.89 to 1.02) for A/C genotype and 0.94 (95% CI = 0.87 to 1.01) for A/A genotype. Conclusions Higher tobacco consumption is associated with higher systemic inflammation both genetically and observationally, whereas systemic inflammation was not associated with airflow limitation genetically. Implications The association between higher tobacco consumption and higher systemic inflammation may be causal, and the association is stronger among current smokers compared to former smokers, indicating that smoking cessation may reduce the effects of smoking on systemic inflammation. Systemic inflammation does not seem to be a causal driver in development of airflow limitation. These findings can help to understand the pathogenic effects of smoking and the interplay between smoking, systemic inflammation, and airflow limitation and hence development and progression of chronic obstructive pulmonary disease.

scholarly journals A Cross-sectional Comparative Study of hs-CRP Levels between Non Diabetic and Diabetic Patients of Chronic Obstructive Pulmonary Disease

2021 ◽  
Author(s):  
Rajesh Sahu ◽  
Ratan Kumar ◽  
Jusmita Dutta ◽  
Gayatri Yadav
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Diabetic Group ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Cross Sectional ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Hs Crp

Introduction: Chronic Obstructive Pulmonary Disease (COPD) is characterised by persistent airflow limitation and is a global health issue with high social and economic burden. Type 2 Diabetes Mellitus (T2DM) is a major global metabolic disorder affecting approximately 300 million individuals worldwide. Accordingly, chronic low grade systemic inflammation is probably one of the common denominators between COPD and T2DM. Aim: To evaluate the status of systemic inflammation in COPD patient with/without T2DM, using quantitative serum high sensitivity C-Reactive Protein (hs-CRP) and Total Leucocyte Count (TLC). Materials and Methods: This cross-sectional study was conducted for a period of one year from May 2019 to April 2020 on 100 patients of COPD patients attending outpatient department. Either known patients of COPD or patients with complains of chronic cough was evaluated with chest x-ray and pulmonary function test (spirometry) after thorough history and physical examination. Global Initiative for Chronic Obstructive Lung Disease-GOLD guidelines a grading system for COPD was used for assessing severity. For assessing diabetes, criteria adopted from American Diabetes Association (ADA) i.e., symptoms of diabetes plus random plasma glucose >200 mg/dL (11.1 mMol/L). Venous blood samples were obtained to perform quantitative hs-CRP estimation by immune turbidimetry method as a marker of systemic inflammation. Statistical analysis was performed using Statistical Package for the Social Sciences (SPSS) version 26.0 of International Business Machines (IBM) Corporation, California, United States of America (USA). Results: The T2DM was present in 40% COPD patients. The frequencies of T2DM in patients with GOLD stages I, II, III, and IV were 16%, 45%, 28%, and 11%, respectively. The mean hs-CRP levels for diabetic group was 5.45±1.07 mg/L, which was significantly higher (p<0.05) than 2.26±0.69 mg/L that of non diabetic group. Conclusion: Present study concluded that the inflammatory process is a definite pathophysiological factor that has a significant link between COPD and T2DM and can be evaluated using a marker like hs-CRP level and TLC.

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.

Screening of High-risk Patients for Chronic Obstructive Pulmonary Disease in Primary Care: A Narrative Review (Preprint)

2020 ◽  
Author(s):  
Ponrathi Athilingam ◽  
Andrew Bugajski ◽  
Usha Menon
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Current Knowledge ◽  
Screening Tools ◽  
Chronic Obstructive ◽  
Early Screening ◽  
Obstructive Pulmonary Disease ◽  
Impaired Lung Function ◽  
Risk Patients

UNSTRUCTURED Chronic obstructive pulmonary disease (COPD) predominantly affects older adults, and claimed 3 million lives in 2016, making it the third leading cause of death worldwide. Over 35 million Americans aged 40 or older have lung function consistent with diagnosable COPD. COPD and cardiovascular disease (CVD) have a bidirectional relationship, in that one is a risk factor for developing the other. National and international consortiums recommend early screening of adults at risk of COPD, such as those with CVD. Recommended screening strategies include screening tools to assess symptoms, medical history, and handheld spirometry. Handheld spirometry has high diagnostic accuracy and if impaired lung function is indicated, these patients are referred for pulmonary function testing (PFT), the diagnostic gold standard for COPD. However, there is no clinical consensus for pulmonary screening in people with CVD. Current knowledge relating to the prevalence and incidence of CVD in people with COPD and the mechanisms that underlie their coexistence is key in combating the global burden of COPD.

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