Eosinophilic Chronic Obstructive Pulmonary Disease

Weissler, Jonathan C.; Adams, Traci N.

doi:10.1007/s00408-021-00492-0

Cited by 11 publications

(8 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Тройную Таблица 1. Основные характеристики пациентов, включенных в исследование 57 (95) 3 (5) 55 (91,7) 5 (8,3) 56 (93,3) 4 (6,7) 0 На момент индексного обострения ХОБЛ в плазме крови пациентов методом твердофазного иммуноферментного анализа определяли маркеры: ■ эозинофильного воспаления: эозинофильный катионный белок (ЕСР), IL-5 [16,23]; ■ нейтрофильного воспаления: нейтрофильная эластаза, гранулоцитарно-макрофагальный колониестимулирущий фактор (GM-CSF) [20,21]: ■ макрофагального воспаления: моноцитарный хемотаксический протеин 1 (МСР-1) [24]; ■ фиброзирования: фактор роста фибробластов 2 (FGF-2), трансформирующий фактор роста бета 1 (TGF-β1), гиалуроновая кислота, N-терминальный пептид проколлагена III типа (PIIINP) [25]; ■ а также уровень матриксных металлопротеиназ (ММР) 1 и 9 изоформ [26], IL-1β, С-реактивного белка (СРБ).…”

Section: материалы и методыunclassified

“…Оценка молекулярного паттерна обострения показала следующие результаты. В группах вирус-ассоциированных и вирусно-бактериальных обострений ХОБЛ в сравнении с бактериальными и контролем наблюдали увеличение концентраций в крови эозинофильного катионного белка, IL-5, что свидетельствует о преобладании воспаления с эозинофилией [16,23] (табл. 3).…”

Section: хронические заболевания легкихunclassified

See 1 more Smart Citation

Clinical and molecular features of virus-induced acute exacerbations of chronic obstructive pulmonary diseas

et al. 2022

View full text Add to dashboard Cite

Introduction. Inflammation in viral-induced acute exacerbations of chronic obstructive pulmonary disease (COPD) is not studied enough.The aim was to establish molecular pattern of inflammation in viral-induced acute exacerbations of chronic obstructive pulmonary disease (AECOPD) in comparison with bacterial AECOPD and to reveal associations with AECOPD phenotype and subsequent COPD progression.Materials and methods. Subjects hospitalized with acute exacerbations of COPD (AECOPD) of which 60 were viral, 60 were bacterial and 60 were viral-bacterial were recruited to single center prospective (52 weeks) cohort study. Control group – 30 healthy people. COPD were diagnosed previously during stable phase of the disease according to spirographic criteria. Viral AECOPD were confirmed by detection of RNA of influenza A and B, respiratory syncytial virus, rhinovirus or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in sputum or bronchoalveolar lavage fluid (BALF) using reverse transcription-polymerase chain reaction (RT-PCR). Bacterial AECOPD were confirmed by sputum/BALF neutrophilia or elevated blood procalcitonin levels or by detecting bacteria by standard culture method. Plasma concentrations of cytokines, fibrotic markers, enzymes were measured by enzyme-linked immunosorbent assay, plasma fibrinogen – by Clauss method. Complex lung function investigation, Dopplerechocardiography, subsequent AECOPD assessment were done. Kruskal-Wallis and chi-square test were used to compare groups, Cox regression and linear regression – to explore relationships.Results. Viral AECOPD were characterized by highest plasma concentrations of Eosinophilic cationic protein (62,3 (52,4; 71,0) ng/ml)), interleukin-5 (IL-5) (11,3 (8,4; 15,9) pg/ml), fibroblast growth factor-2 (FGF-2) (10,4 (6,2; 14,9) pg/ml), transforming growth factor-β1 (TGF-β1) (922,4 (875,7; 953,8) pg/ml), hyaluronic acid (185,4 (172,8; 196,3) ng/ml), amino-terminal propeptide of type III procollagen (PIIINP) (249,2 (225,1; 263,7) ng/ml), matrix metalloproteinase-1 (MMP-1) (235,2 (208,6; 254,9) pg/ml). Levels of IL-5 during AE COPD was the predictor of FEV1, bronchodilation coefficient, subsequent exacerbations at remote period, fibrinogen was associated with FEV1, PIIINP and FGF-2 with DLco, PaO2, mean pulmonary artery pressure (mPAP), exacerbations, MMP-1 – with mPAP.Conclusions. In virus-induced AECOPD inflammation pattern differed from those in bacterial one and associated with AECOPD phenotype and COPD phenotype at the stable phase.

show abstract

Section: материалы и методыunclassified

Section: хронические заболевания легкихunclassified

Clinical and molecular features of virus-induced acute exacerbations of chronic obstructive pulmonary diseas

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Легочная гипертензия является частым осложнением ХОБЛ и обычно возникает в результате фиброза стенки сосуда [18]. Другими ассоциациями, обнаруженными для этой группы, был IL-5 [19], связанный с эозинофильным типом воспаления, и MMP-9, участвующий в разрушении внеклеточного матрикса соединительной ткани легких [20], что и предполагало связь с отношением остаточного объема легких к общей емкости легких.…”

Section: результаты и обсуждениеunclassified

Clinical and Functional, Cellular and Molecular Characteristics of Occupational Chronic Obstructive Pulmonary Disease Depending on the Composition of Unintentional Nanoparticles

Shpagina¹,

Zenkova²,

Shpagin³

et al. 2022

SMV

View full text Add to dashboard Cite

Introduction. Occupational chronic obstructive pulmonary disease (OCOPD) is characterized by steadily progressive persistent bronchial obstruction and emphysema, which leads to disability and reduced life expectancy of patients. Industrial aerosols are one of the main occupational health risks. According to Federal State Statistics Service, 4.5% of all workers are exposed to aerosols of predominantly fibrogenic action, 7.7% – to a chemical factor. At present, the determination of the physicochemical properties of nanoparticles and the study of their effect on the phenotype of occupational bronchopulmonary pathology are still insufficiently studied. Aim of the research. To identify clinical, functional, cellular and molecular features of the phenotype of occupational chronic obstructive pulmonary disease under exposure to aerosols with unintentional nanoparticles of various compositions. Materials and methods. A single-center cohort study was performed. Patients with OCOPD (GOLD 2011-2021 criteria) who worked under conditions of exposure to aerosols containing unintentional nanoparticles were included (n = 70). Comparison group – COPD due to tobacco smoking (n = 70), control – conditionally healthy (n = 70). The groups are comparable in terms of demographic indicators, duration of the disease. Nanoparticles in the air of the working area were determined by inductively coupled plasma atomic emission spectrometry (ICP-AES) and scanning electron microscopy. At the workplaces, in 36 persons, the mass concentration of metal nanoparticles was the highest, in 34 persons – that of silica nanoparticles. Spirography, body plethysmography, assessment of the diffusing capacity of the lungs (DLco/Va) for carbon monoxide (DLco/Va), cytological examination of induced sputum were performed. Markers of cellular inflammation and fibrosis were studied: interleukin-1β (IL1-β), interleukin-5 (IL-5), C-reactive protein (CRP), fibroblast growth factor-2 (FGF-2), transforming growth factor-β1 (TGF-β1), procollagen type 3 N-terminal propeptide (PIIINP), matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-9 (MMP-9), soluble vascular cell adhesion molecule-1 (sVCAM 1) and distribution subpopulations of blood monocytes by flow cytometry. Correlations were determined by the method of linear regression. Results. The clinical and functional peculiar characteristics of COPD when exposed to aerosols with metal nanoparticles are: the greatest severity of dyspnea according to mMRC scale 2.35 ± 0.120 points, dry cough with paroxysms 75.0%, low quality of life 70.8 ± 5.68 points, ventilation function of the lungs with the greatest severity of bronchial obstruction (Raw 0.66 kPa s/l, FEV1 36%) and static pulmonary hyperinflation (functional residual capacity (FRC) 192%, residual volume of the lungs (PRV) 187%), maximum pulmonary hypertension (37 mm Hg), the lowest values of DLco 36%. The cellular and molecular composition in OCOPD from exposure to metal nanoparticles is characterized by: eosinophilic type of inflammation 47.2%, the highest level of classical monocytes 95.4%, high expression of CCR5 21.56%, elevated serum concentrations of PIIINP 156.7 ± 15.23 ng/mL, IL-5 2.1 ± 0.42 pg/mL and MMP-9 346.2 ± 31.74 pg/mL. In COPD due to expose to industrial aerosols containing silica nanoparticles, the disease is characterized by the least severity of dyspnea mMRC 1.64 ± 0.118 points, the presence of a pronounced dry cough 61.7%, a significant decrease in DLco/Va (47%) with the least severity of bronchial obstruction (Raw 0.51 kPa s/l, FEV1 56%) and pulmonary hyperinflation. The cellular and molecular features of COPD from exposure to silica nanoparticles include: paucigranulocytic type of inflammation 44.1%, the lar¬gest proportion of non-classical CD14DimCD16+ monocytes – 21.1%, a significant level of CCR2 expression 11.10%, elevated serum concentrations of PIIINP 92, 1 ± 9.32ng/mL, FGF-2 16.1 ± 3.51pg/mL and sVCAM-1 46.1 ± 9.15 pg/mL. Reliable correlations between the mass concentrations of metal nanoparticles and classical monocytes (B = 1.6), silicon nanoparticles and nonclassical monocytes (B = 1.2) were determined. At the same time, classic monocytes were significant predictors of DLco (B = –1.7), functional residual lung capacity (B = 1.3), mean pulmonary artery pressure (B = –1.6), inflammation with eosinophilia (B = 1.2), non-classical monocytes – DLco (B = –1.4), paucigranulocytic inflammation (B = 1.3), p < 0.015. In the linear regression model, the mass concentration of metal nanoparticles is associated with the N-terminal propeptide of type 3 procollagen, interleukin-5, and matrix metalloproteinase-9. Serum PIIINP concentrations were associated with carbon monoxide diffusing capacity (DLco), IL-5 – with eosinophilic airway inflammation, and MMP-9 – with residual volume of lungs/total lung capacity (RV/TLC) ratio. The mass concentration of silica nanoparticles was associated with PIIINP, FGF-2 and sVCAM-1. In turn, the N-terminal propeptide of procollagen type 3 was associated with DLco, mean pulmonary artery pressure (MPAP); fibroblast growth factor-2 – with DLco, and sVCAM-1 – with MPAP (p < 0.01). Conclusion. Under conditions of exposure to industrial aerosol, various phenotypes of chronic obstructive pulmonary disease are formed depending on the composition of unintentional nanoparticles.

show abstract

“…In keeping with initially stated goals [ 1 ], we published ten State-of-the Art review articles in our six issues of 2021 [ 2 – 11 ]. State-of-the-Art reviews are comprehensive, up-to-date reviews on specific topics contributed by experts in the field.…”

mentioning

confidence: 99%

“…Obstructive airways disease was again well represented in the journal. An eclectic collection of published articles examined various aspects of chronic obstructive pulmonary disease and asthma [ 2 , 11 , 15 , 31 , 55 , 64 , 69 – 73 ].…”

mentioning

confidence: 99%

LUNG Year in Review: 2021

Dicpinigaitis

2022

Lung

View full text Add to dashboard Cite

Eosinophilic Chronic Obstructive Pulmonary Disease

Cited by 11 publications

References 57 publications

Clinical and molecular features of virus-induced acute exacerbations of chronic obstructive pulmonary diseas

Clinical and molecular features of virus-induced acute exacerbations of chronic obstructive pulmonary diseas

Clinical and Functional, Cellular and Molecular Characteristics of Occupational Chronic Obstructive Pulmonary Disease Depending on the Composition of Unintentional Nanoparticles

LUNG Year in Review: 2021

Contact Info

Product

Resources

About