scholarly journals Effect of the combination of theophylline and budesonide on production of proinflammatory cytokines by blood cells of patients with chronic obstructive pulmonary disease

2021 ◽  
Vol 99 (10) ◽  
pp. 14-22
Author(s):  
A. G. Kadushkin ◽  
A. D. Taganovich ◽  
L. V. Movchan ◽  
E. I. Talabaeva ◽  
A. V. Plastinina ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
T Lymphocytes ◽  
Pulmonary Disease ◽  
Cytotoxic T Lymphocytes ◽  
Proinflammatory Cytokines ◽  
Blood Cells ◽  
Mononuclear Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
T Helpers

The objective: to evaluate the ability of the combination of theophylline and budesonide to suppress proinflammatory cytokine production byblood cells in patients with chronic obstructive pulmonary disease (COPD).Subjects and Methods. Peripheral blood mononuclear cells (PBMCs) or whole blood cells of COPD patients (n = 27) were incubated with budesonide (10 nM), theophylline (1 μM), or the combination thereof and stimulated with phytohemagglutinin (PHA) or phorbol myristate acetate (PMA) and ionomycin. The enzyme immunoassay was used to evaluate the secretion of thymic stromal lymphopoietin (TSLP), macrophage migration inhibitory factor (MIF), interleukin 17A (IL-17A), IL-33, and other mediators of PBMC cells, and induced PHA. The flow cytometry was used to analyze intracellular production of proinflammatory cytokines stimulated by PMA/ionomycin in T-helpers (CD4+) and cytotoxic T-lymphocytes (CD8+).Results. Theophylline reduced the secretion of IL-4 and IL-17A by PBMC cells. The combination of budesonide with theophylline inhibited the synthesis of IL-4, IL-5, IL-8, IL-13, IL-17A, IL-33, TSLP, MIF by PBMC cells as well as the production of IL-4, IL-8, tumor necrosis factor-α, and interferon-γ by cytotoxic T-lymphocytes and T-helpers. The combination of theophylline and budesonide had a more pronounced inhibitory effect on the production of IL-4 and IL-8 by PBMC cells as well as the synthesis of IL-4 by CD4+ T-cells and IL8 by CD8+ T-lymphocytes versus the effect of monotherapy with budesonide.

scholarly journals Methylation of SERPINA1 gene promoter may predict chronic obstructive pulmonary disease in patients affected by acute coronary syndrome

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
John Charles Rotondo ◽  
Giorgio Aquila ◽  
Lucia Oton-Gonzalez ◽  
Rita Selvatici ◽  
Paola Rizzo ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Acute Coronary Syndrome ◽  
Pulmonary Disease ◽  
Blood Cells ◽  
Gene Promoter ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Coronary Syndrome ◽  
Copd Patients ◽  
Potential Biomarker

Abstract Background Diagnostic biomarkers for detecting chronic obstructive pulmonary disease (COPD) in acute coronary syndrome (ACS) patients are not available. SERPINA1, coding for the most potent circulating anti-inflammatory protein in the lung, has been found to be differentially methylated in blood cells from COPD patients. This study aimed to investigate the methylation profile of SERPINA1 in blood cells from ACS patients, with (COPD+) or without COPD (COPD−). Methods Blood samples were from 115 ACS patients, including 30 COPD+ and 85 COPD− according to lung function phenotype, obtained with spirometry. DNA treated with sodium bisulfite was PCR-amplified at SERPINA1 promoter region. Methylation analysis was carried out by sequencing the PCR products. Lymphocytes count in ACS patients was recorded at hospital admission and discharge. Results SERPINA1 was hypermethylated in 24/30 (80%) COPD+ and 48/85 (56.5%) COPD− (p < 0.05). Interestingly, at hospital discharge, lymphocytes count was higher in COPD− patients carrying SERPINA1 hypermethylated (1.98 × 103 ± 0.6 cell/µl) than in COPD− carrying SERPINA1 hypomethylated (1.7 × 103 ± 0.48 cell/µl) (p < 0.05). Conclusions SERPINA1 is hypermethylated in blood cells from COPD+ patients. COPD− carrying SERPINA1 hypermethylated and high lymphocytes count may be at risk of COPD development. Therefore, SERPINA1 hypermethylation may represent a potential biomarker for predicting COPD development in ACS patients.

scholarly journals New Insights into the Implication of Mitochondrial Dysfunction in Tissue, Peripheral Blood Mononuclear Cells, and Platelets during Lung Diseases

2020 ◽  
Vol 9 (5) ◽  
pp. 1253 ◽  
Author(s):  
Marianne Riou ◽  
Abrar Alfatni ◽  
Anne-Laure Charles ◽  
Emmanuel Andrès ◽  
Cristina Pistea ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Arterial Hypertension ◽  
Blood Cells ◽  
Lung Diseases ◽  
Mononuclear Cells ◽  
Chronic Obstructive ◽  
Peripheral Blood Mononuclear ◽  
Obstructive Pulmonary Disease ◽  
Blood Mononuclear Cells ◽  
Pulmonary Arterial

Lung diseases such as chronic obstructive pulmonary disease, asthma, pulmonary arterial hypertension, or idiopathic pulmonary fibrosis are major causes of morbidity and mortality. Complex, their physiopathology is multifactorial and includes lung mitochondrial dysfunction and enhanced reactive oxygen species (ROS) release, which deserves increased attention. Further, and importantly, circulating blood cells (peripheral blood mononuclear cells-(PBMCs) and platelets) likely participate in these systemic diseases. This review presents the data published so far and shows that circulating blood cells mitochondrial oxidative capacity are likely to be reduced in chronic obstructive pulmonary disease (COPD), but enhanced in asthma and pulmonary arterial hypertension in a context of increased oxidative stress. Besides such PBMCs or platelets bioenergetics modifications, mitochondrial DNA (mtDNA) changes have also been observed in patients. These new insights open exciting challenges to determine their role as biomarkers or potential guide to a new therapeutic approach in lung diseases.

Oxidative stress and damage to erythrocytes in patients with chronic obstructive pulmonary disease — changes in ATPase and acetylcholinesterase activity

2015 ◽  
Vol 93 (6) ◽  
pp. 574-580 ◽  
Author(s):  
Bożena Bukowska ◽  
Paulina Sicińska ◽  
Aneta Pająk ◽  
Aneta Koceva-Chyla ◽  
Tadeusz Pietras ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Red Blood Cells ◽  
Pulmonary Disease ◽  
Blood Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Membrane Enzymes ◽  
Copd Patients ◽  
The Impact

The study indicates, for the first time, the changes in both ATPase and AChE activities in the membrane of red blood cells of patients diagnosed with COPD. Chronic obstructive pulmonary disease (COPD) is one of the most common and severe lung disorders. We examined the impact of COPD on redox balance and properties of the membrane of red blood cells. The study involved 30 patients with COPD and 18 healthy subjects. An increase in lipid peroxidation products and a decrease in the content of -SH groups in the membrane of red blood cells in patients with COPD were observed. Moreover, an increase in the activity of glutathione peroxidase and a decrease in superoxide dismutase, but not in catalase activity, were found as well. Significant changes in activities of erythrocyte membrane enzymes in COPD patients were also evident demonstrated by a considerably lowered ATPase activity and elevated AChE activity. Changes in the structure and function of red blood cells observed in COPD patients, together with changes in the activity of the key membrane enzymes (ATPases and AChE), can result from the imbalance of redox status of these cells due to extensive oxidative stress induced by COPD disease.

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