Cigarette Smoking Acutely Decreases Serum Levels of the Chronic Obstructive Pulmonary Disease Biomarker sRAGE

2018 ◽  
Vol 198 (11) ◽  
pp. 1456-1458 ◽  
Author(s):  
Simon D. Pouwels ◽  
Frank Klont ◽  
Marcel Kwiatkowski ◽  
Valerie R. Wiersma ◽  
Alen Faiz ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Cigarette Smoking ◽  
Pulmonary Disease ◽  
Serum Levels ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Disease Biomarker

Oxidized low-density lipoproteins and its connection with dyslipidemia, inflammatory markers, and oxidative stress in patients with occupational chronic obstructive pulmonary disease

2021 ◽  
Vol 31 (4) ◽  
pp. 456-462
Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova ◽  
V. V. Troshin ◽  
V. D. Fedotov
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Comparison Group ◽  
Serum Levels ◽  
Low Density Lipoproteins ◽  
Chronic Obstructive ◽  
Low Density ◽  
Obstructive Pulmonary Disease ◽  
Occupational Copd

The role of low-density oxidized lipoproteins (OxLDL) in the pathogenesis of occupational chronic obstructive pulmonary disease (COPD) is not understood well enough.The study aims to determine the serum levels of oxidized low-density lipoproteins and their relationship with lipid profile, the level of oxidative stress and level C-reactive protein in patients with occupational chronic obstructive pulmonary disease.Methods. 116 patients diagnosed with occupational COPD and 25 patients with no respiratory diseases (comparison group) were examined. Serum levels of OxLDL was determined by solid phase enzyme-linked immunosorbent assay (ELISA) using the commercial reagent kit MDA-oxLDL from Biomedica Gruppe, Austria.Results. Circulating OxLDL was detected in serum in a significant proportion of patients with stable occupational COPD. In most of the patients, the concentration of OxLDL was within the values observed in the comparison group or exceeded them by no more than two times. In the minority of patients with occupational COPD (16.5%), the concentration of OxLDL was high and 4 – 10 times higher than its average value in the comparison group. It can be assumed that the revealed differences in the concentration of OxLDL are due to the different degree and intensity of oxidation of low-density lipoproteins. The relationships between OxLDL and lipid metabolism, oxidative stress (OS), the antioxidant capacity of serum (AOS), and serum levels of C-reactive protein were described.Conclusion. Serum OxLDL levels in patients with occupational COPD, the relationship between OxLDL and lipid metabolism, oxidative stress, and inflammation will provide an expanded view of the pathogenetic aspects of occupational COPD.

scholarly journals Changes in Th1/Th2-producing cytokines during acute exacerbation chronic obstructive pulmonary disease

2018 ◽  
Vol 46 (9) ◽  
pp. 3890-3902 ◽  
Author(s):  
Bing Wei ◽  
Chun Sheng Li
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Acute Exacerbation ◽  
Chronic Obstructive Lung Disease ◽  
Serum Levels ◽  
T Cell Subsets ◽  
Th2 Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Ifn Γ

Objective This study aimed to explore cytokine serum levels and the ratio of type 1 T helper (Th1)/Th2 cells in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Methods A total 245 patients diagnosed with AECOPD and 193 patients who progressed to stable COPD after the initiation of treatment in hospital were selected, while a further 50 healthy individuals served as controls. All patients with COPD were diagnosed using Global Initiative for Chronic Obstructive Lung Disease criteria. Serum concentrations of interleukin (IL)-2, interferon (IFN)-γ, IL-4, IL-10, IL-17, and immunoglobulin (Ig)E were measured using enzyme-linked immunosorbent assays. Results AECOPD patients had higher levels of IL-2, IFN-γ, IL-4, IL-10, IL-17, and IgE than those with stable COPD or controls. Intriguingly, the ratios of Th1/Th2 and IL-17/IgE were lower in AECOPD patients compared with the other two groups. These data suggest that AECOPD patients produce more IgE and have more differentiated Th2 cells than other groups. Conclusion Our findings suggest that an imbalance of circulating CD4+ T cell subsets correlates with AECOPD, and that a shift of Th1/Th2 and IL-17/IgE ratios may be caused by increased Th2 cell production.

Increased IL-33 expression in chronic obstructive pulmonary disease

2015 ◽  
Vol 308 (7) ◽  
pp. L619-L627 ◽  
Author(s):  
Jie Xia ◽  
Junling Zhao ◽  
Jin Shang ◽  
Miao Li ◽  
Zhilin Zeng ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Cell Activation ◽  
Critical Role ◽  
Serum Levels ◽  
Peripheral Blood Lymphocytes ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Interleukin 33 ◽  
Cellular Source

Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by inflammatory cell activation and the release of inflammatory mediators. Interleukin-33 (IL-33) plays a critical role in various inflammatory and immunological pathologies, but evidence for its role in COPD is lacking. This study aimed to investigate the expression of IL-33 in COPD and to determine whether IL-33 participates in the initiation and progression of COPD. Levels of serum IL-33 and its receptors were measured by ELISA, and serum levels of IL-33, ST2, and IL-1 receptor accessory protein were elevated in patients with COPD compared with control subjects. Flow cytometry analysis further demonstrated an increase in peripheral blood lymphocytes (PBLs) expressing IL-33 in patients with COPD. Immunofluorescence analysis revealed that the main cellular source of IL-33 in lung tissue was human bronchial epithelial cells (HBEs). Cigarette smoke extract and lipopolysaccharide could enhance the ability of PBLs and HBEs to express IL-33. Furthermore, PBLs from patients with COPD showed greater IL-33 release in response to the stimulus. Collectively, these findings suggest that IL-33 expression levels are increased in COPD and related to airway and systemic inflammation. Therefore, IL-33 might contribute to the pathogenesis and progression of this disease.

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