Inflammatory responses to incremental exercise in chronic obstructive pulmonary disease

2021 ◽  
Author(s):  
Aslihan Cakmak ◽  
Deniz Inal-Ince ◽  
Elif Kocaaga ◽  
Ipek Baysal ◽  
Samiye Yabanoglu-Ciftci ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Inflammatory Responses ◽  
Incremental Exercise ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease

2015 ◽  
Vol 8 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Chang Min Yoon ◽  
Milang Nam ◽  
Yeon-Mok Oh ◽  
Charles S. Dela Cruz ◽  
Min-Jong Kang
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Inflammatory Responses ◽  
Pulmonary Inflammation ◽  
Innate Immune ◽  
Western Society ◽  
Future Research ◽  
Chronic Obstructive ◽  
Inflammasome Activation ◽  
Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is characterized by enhanced chronic airway and lung inflammatory responses to noxious particles or gases. It is a major unmet medical need worldwide, and in Western society is strongly associated with exposure to cigarette smoke (CS). CS-induced inflammation is believed to be a key immune driver in the pathogenesis of COPD. Since the concept of inflammasomes was first introduced nearly a decade ago, these have been increasingly recognized as a central player in innate immune and inflammatory responses. In addition, studies have emerged demonstrating that mitochondrial innate immune signaling plays an important role in CS-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. Here, recent discoveries about inflammasome activation and mitochondrial biology and their role in COPD pathogenesis are reviewed. In addition, the current limitations of our understanding of this theme and future research directions are discussed.

scholarly journals Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease

2020 ◽  
Vol 53 (1) ◽  
pp. 135-150
Author(s):  
Silvestro Ennio D’Anna ◽  
Mauro Maniscalco ◽  
Francesco Cappello ◽  
Mauro Carone ◽  
Andrea Motta ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Viral Infections ◽  
Inflammatory Responses ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

PI3K/Akt-Nrf2 and Anti-Inflammation Effect of Macrolides in Chronic Obstructive Pulmonary Disease

2019 ◽  
Vol 20 (4) ◽  
pp. 301-304 ◽  
Author(s):  
Xuejiao Sun ◽  
Lin Chen ◽  
Zhiyi He
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Inflammatory Responses ◽  
Protective Role ◽  
Akt Pathway ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Inflammatory Mechanism

Background: Chronic Obstructive Pulmonary Disease (COPD) is a systematic inflammatory disease, and smoking is an important risk factor for COPD. Macrolide can reduce COPD inflammation. However, the inflammatory mechanism of COPD remains unclear and the anti-inflammatory mechanism of Macrolide is complex and not exactly known. Methods: We read and analysed thirty-eight articles, including original articles and reviews. Results: The expression of Nrf2 was lower in COPD patients and might have a protective role against apoptosis caused by CSE-induced oxidative stress. Nrf2 may play an important role in COPD inflammation. Nrf2 is a key factor in downstream of PI3K/Akt and is involved in the regulation of oxidative stress and inflammatory response. Therefore, PI3K/Akt pathway may play an important role in the activation of Nrf2 and COPD inflammation. Macrolide reduces lung and systemic inflammation of COPD by regulating PI3K/Akt pathway. Conclusion: This review indicates that PI3K/Ak-Nrf2 may play an important role in COPD inflammation and macrolides may reduce lung and systemic inflammation of COPD by regulating PI3K/Akt-Nrf2 pathway. However, many crucial and essential questions remain to be answered. Further understanding of the mechanisms of macrolide efficacy and PI3K/Akt-Nrf2-mediated inflammatory responses may provide a new clue for exploring COPD treatment in the future.

scholarly journals Chemerin: A Potential Regulator of Inflammation and Metabolism for Chronic Obstructive Pulmonary Disease and Pulmonary Rehabilitation

2020 ◽  
Vol 2020 ◽  
pp. 1-20
Author(s):  
Jian Li ◽  
Yufan Lu ◽  
Ning Li ◽  
Peijun Li ◽  
Zhengrong Wang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lipid Metabolism ◽  
Pulmonary Disease ◽  
Inflammatory Responses ◽  
Therapeutic Interventions ◽  
Chronic Obstructive ◽  
Barrier Dysfunction ◽  
Obstructive Pulmonary Disease ◽  
Glucose And Lipid Metabolism

Chronic obstructive pulmonary disease (COPD) features chronic inflammatory reactions of both intra- and extrapulmonary nature. Moreover, COPD is associated with abnormal glucose and lipid metabolism in patients, which influences the prognosis and chronicity of this disease. Abnormal glucose and lipid metabolism are also closely related to inflammation processes. Further insights into the interactions of inflammation and glucose and lipid metabolism might therefore inspire novel therapeutic interventions to promote lung rehabilitation. Chemerin, as a recently discovered adipokine, has been shown to play a role in inflammatory response and glucose and lipid metabolism in many diseases (including COPD). Chemerin recruits inflammatory cells to sites of inflammation during the early stages of COPD, leading to endothelial barrier dysfunction, early vascular remodeling, and angiogenesis. Moreover, it supports the recruitment of antigen-presenting cells that guide immune cells as part of the body’s inflammatory responses. Chemerin also regulates metabolism via activation of its cognate receptors. Glucose homeostasis is affected via effects on insulin secretion and sensitivity, and lipid metabolism is changed by increased transformation of preadipocytes to mature adipocytes through chemerin-binding receptors. Controlling chemerin signaling may be a promising approach to improve various aspects of COPD-related dysfunction. Importantly, several studies indicate that chemerin expression in vivo is influenced by exercise. Although available evidence is still limited, therapeutic alterations of chemerin activity may be a promising target of therapeutic approaches aimed at the rehabilitation of COPD patients based on exercises. In conclusion, chemerin plays an essential role in COPD, especially in the inflammatory responses and metabolism, and has a potential to become a target for, and a biomarker of, curative mechanisms underlying exercise-mediated lung rehabilitation.

Systemic oxygen extraction during incremental exercise in patients with severe chronic obstructive pulmonary disease

1998 ◽  
Vol 78 (3) ◽  
pp. 201-207 ◽  
Author(s):  
David A. Oelberg ◽  
Benjamin D. Medoff ◽  
Deborah H. Markowitz ◽  
Paul P. Pappagianopoulos ◽  
Leo C. Ginns ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Incremental Exercise ◽  
Oxygen Extraction ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Systemic Oxygen

scholarly journals Different Patterns of Lung Sirtuin Expression in Smokers With and Without Chronic Obstructive Pulmonary Disease

Medicina ◽  
2012 ◽  
Vol 48 (10) ◽  
pp. 80 ◽  
Author(s):  
Sergejs Isajevs ◽  
Gunta Strazda ◽  
Uldis Kopeika ◽  
Immanuels Taivans
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Inflammatory Responses ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Small Airways ◽  
Obstructive Pulmonary Disease ◽  
Nonhistone Proteins ◽  
Proinflammatory Mediators ◽  
Large Airways

Background and Objective. Chronic obstructive pulmonary disease is characterized by persistent and modified inflammatory responses in lung. Human sirtuin, an antiaging and antiinflammatory protein, is a metabolic NAD(+)-dependent protein/histone deacetylase that regulates proinflammatory mediators by deacetylating histone and nonhistone proteins. The aim of our study was to compare the expression of sirtuin in large and small airways in nonsmokers, asymptomatic smokers, and smokers with chronic obstructive pulmonary disease. Material and Methods. A total of 12 nonsmokers, 14 asymptomatic smokers, and 12 smokers with moderate chronic obstructive pulmonary disease were enrolled into the study. Immunohistochemical and Western blot methods were used to analyze sirtuin expression in the airways. Results. The obtained results showed the nonuniform sirtuin expression throughout the bronchial tree. Smokers both with and without chronic obstructive pulmonary disease had decreased sirtuin expression in large airways. However, in small airways, sirtuin expression was decreased only in patients with chronic obstructive pulmonary disease. In addition, a correlation between airflow limitation, smoked pack-years and the number of sirtuin-positive cells in airways was found. Conclusions. Smoking is characterized by suppressed sirtuin expression in large airways, whereas chronic obstructive pulmonary disease is characterized by more severe suppression of sirtuin expression both in large and small airways.

scholarly journals The Involvement of PDE4 in the Protective Effects of Melatonin on Cigarette-Smoke-Induced Chronic Obstructive Pulmonary Disease

Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6588
Author(s):  
Je-Oh Lim ◽  
Woong-Il Kim ◽  
Se-Jin Lee ◽  
So-Won Pak ◽  
Young-Kwon Cho ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Inflammatory Responses ◽  
Chronic Obstructive ◽  
Melatonin Treatment ◽  
Obstructive Pulmonary Disease ◽  
Camp Levels

Chronic obstructive pulmonary disease (COPD) is a significant disease threatening human health. Currently, roflumilast, a phosphodiesterase (PDE)4 inhibitor, is recommended as a therapeutic agent for COPD. In this study, we investigated the therapeutic effects of melatonin against COPD, focusing on determining whether it is a PDE4 inhibitor via in vivo and in vitro experiment using cigarette smoke (CS) and cigarette smoke condensate (CSC), respectively. In the in vivo experiments, melatonin treatment reduced inflammatory responses, including inflammatory cell counts. Melatonin treatment also suppressed the CS-exposure-induced upregulation of cytokine and matrix metalloproteinase (MMP)-9, reduced the PDE4B expression, and elevated cAMP levels. In addition, these effects were synergistic, as melatonin and roflumilast cotreatment eventually ameliorated the CS-exposure-induced worsening of lung function. In the CSC-stimulated NCI-H292 cells, melatonin inhibited elevation in the levels of inflammatory cytokines, MMP-9, and PDE4, and elevated cAMP levels. Furthermore, melatonin and roflumilast cotreatment was more effective on inflammatory responses than only melatonin or roflumilast treatment. Our results indicate that melatonin relieves inflammatory response and loss of lung function in COPD, which is associated with decreased PDE4 expression. Therefore, we suggest that melatonin is a putative candidate for the treatment of COPD.

Sign in / Sign up

Export Citation Format

Share Document