scholarly journals Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease

2021 ◽  
Vol 22 (14) ◽  
pp. 7634
Author(s):  
Stanislav Kotlyarov ◽  
Anna Kotlyarova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lipid Metabolism ◽  
Pulmonary Disease ◽  
Plasma Membranes ◽  
Molecular Mechanisms ◽  
Bacterial Colonization ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Exacerbations ◽  
Lipid Metabolism Disorders

Exacerbations largely determine the character of the progression and prognosis of chronic obstructive pulmonary disease (COPD). Exacerbations are connected with changes in the microbiological landscape in the bronchi due to a violation of their immune homeostasis. Many metabolic and immune processes involved in COPD progression are associated with bacterial colonization of the bronchi. The objective of this review is the analysis of the molecular mechanisms of lipid metabolism and immune response disorders in the lungs in COPD exacerbations. The complex role of lipid metabolism disorders in the pathogenesis of some infections is only beginning to be understood, however, there are already fewer and fewer doubts even now about its significance both in the pathogenesis of infectious exacerbations of COPD and in general in the progression of the disease. It is shown that the lipid rafts of the plasma membranes of cells are involved in many processes related to the detection of pathogens, signal transduction, the penetration of pathogens into the cell. Smoking disrupts the normally proceeded processes of lipid metabolism in the lungs, which is a part of the COPD pathogenesis.

scholarly journals Lipid Metabolism Disorders in the Comorbid Course of Nonalcoholic Fatty Liver Disease and Chronic Obstructive Pulmonary Disease

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2978
Author(s):  
Stanislav Kotlyarov ◽  
Aleksei Bulgakov
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Pulmonary Disease ◽  
Fatty Liver Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Alcoholic Fatty Liver ◽  
Lipid Metabolism Disorders

Non-alcoholic fatty liver disease (NAFLD) is currently among the most common liver diseases. Unfavorable data on the epidemiology of metabolic syndrome and obesity have increased the attention of clinicians and researchers to the problem of NAFLD. The research results allow us to emphasize the systemicity and multifactoriality of the pathogenesis of liver parenchyma lesion. At the same time, many aspects of its classification, etiology, and pathogenesis remain controversial. Local and systemic metabolic disorders are also a part of the pathogenesis of chronic obstructive pulmonary disease and can influence its course. The present article analyzes the metabolic pathways mediating the links of impaired lipid metabolism in NAFLD and chronic obstructive pulmonary disease (COPD). Free fatty acids, cholesterol, and ceramides are involved in key metabolic and inflammatory pathways underlying the pathogenesis of both diseases. Moreover, inflammation and lipid metabolism demonstrate close links in the comorbid course of NAFLD and COPD.

scholarly journals Bacterial Infection in Chronic Obstructive Pulmonary Disease in 2000: a State-of-the-Art Review

2001 ◽  
Vol 14 (2) ◽  
pp. 336-363 ◽  
Author(s):  
Sanjay Sethi ◽  
Timothy F. Murphy
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Bacterial Infection ◽  
Pulmonary Disease ◽  
Molecular Mechanisms ◽  
Vaccine Development ◽  
Bacterial Colonization ◽  
The United States ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

SUMMARY Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States. The precise role of bacterial infection in the course and pathogenesis of COPD has been a source of controversy for decades. Chronic bacterial colonization of the lower airways contributes to airway inflammation; more research is needed to test the hypothesis that this bacterial colonization accelerates the progressive decline in lung function seen in COPD (the vicious circle hypothesis). The course of COPD is characterized by intermittent exacerbations of the disease. Studies of samples obtained by bronchoscopy with the protected specimen brush, analysis of the human immune response with appropriate immunoassays, and antibiotic trials reveal that approximately half of exacerbations are caused by bacteria. Nontypeable Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae are the most common causes of exacerbations, while Chlamydia pneumoniae causes a small proportion. The role of Haemophilus parainfluenzae and gram-negative bacilli remains to be established. Recent progress in studies of the molecular mechanisms of pathogenesis of infection in the human respiratory tract and in vaccine development guided by such studies promises to lead to novel ways to treat and prevent bacterial infections in COPD.

scholarly journals The Role of ABC Transporters in Lipid Metabolism and the Comorbid Course of Chronic Obstructive Pulmonary Disease and Atherosclerosis

2021 ◽  
Vol 22 (13) ◽  
pp. 6711
Author(s):  
Stanislav Kotlyarov ◽  
Anna Kotlyarova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lipid Metabolism ◽  
Pulmonary Disease ◽  
Abc Transporters ◽  
Large Family ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Lipid Metabolism Disorders ◽  
Transporter Family

Chronic obstructive pulmonary disease (COPD) ranks among the leading causes of morbidity and mortality worldwide. COPD rarely occurs in isolation and is often combined with various diseases. It is considered that systemic inflammation underlies the comorbid course of COPD. The data obtained in recent years have shown the importance of violations of the cross-links of lipid metabolism and the immune response, which are links in the pathogenesis of both COPD and atherosclerosis. The role of lipid metabolism disorders in the pathogenesis of the comorbid course of COPD and atherosclerosis and the participation of ATP-binding cassette (ABC) transporters in these processes is discussed in this article. It is known that about 20 representatives of a large family of ABC transporters provide lipid homeostasis of cells by moving lipids inside the cell and in its plasma membrane, as well as removing lipids from the cell. It was shown that some representatives of the ABC-transporter family are involved in various links of the pathogenesis of COPD and atherosclerosis, which can determine their comorbid course.

scholarly journals Bioinformatic Analysis of ABCA1 Gene Expression in Smoking and Chronic Obstructive Pulmonary Disease

Membranes ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 674
Author(s):  
Stanislav Kotlyarov ◽  
Anna Kotlyarova
Keyword(s):  
Gene Expression ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Alveolar Macrophages ◽  
Plasma Membranes ◽  
Bioinformatic Analysis ◽  
Transport Processes ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Abca1 Gene

Smoking is a key modifiable risk factor for developing the chronic obstructive pulmonary disease (COPD). When smoking, many processes, including the reverse transport of cholesterol mediated by the ATP binding cassette transporter A1 (ABCA1) protein are disrupted in the lungs. Changes in the cholesterol content in the lipid rafts of plasma membranes can modulate the function of transmembrane proteins localized in them. It is believed that this mechanism participates in increasing the inflammation in COPD. Methods: Bioinformatic analysis of datasets from Gene Expression Omnibus (GEO) was carried out. Gene expression data from datasets of alveolar macrophages and the epithelium of the respiratory tract in smokers and COPD patients compared with non-smokers were used for the analysis. To evaluate differentially expressed genes, bioinformatic analysis was performed in comparison groups using the limma package in R (v. 4.0.2), and the GEO2R and Phantasus tools (v. 1.11.0). Results: The conducted bioinformatic analysis showed changes in the expression of the ABCA1 gene associated with smoking. In the alveolar macrophages of smokers, the expression levels of ABCA1 were lower than in non-smokers. At the same time, in most of the airway epithelial datasets, gene expression did not show any difference between the groups of smokers and non-smokers. In addition, it was shown that the expression of ABCA1 in the epithelial cells of the trachea and large bronchi is higher than in small bronchi. Conclusions: The conducted bioinformatic analysis showed that smoking can influence the expression of the ABCA1 gene, thereby modulating lipid transport processes in macrophages, which are part of the mechanisms of inflammation development.

scholarly journals Prevention of COPD exacerbations: medications and other controversies

2015 ◽  
Vol 1 (1) ◽  
pp. 00011-2015 ◽  
Author(s):  
Jørgen Vestbo ◽  
Peter Lange
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Short Review ◽  
Chronic Obstructive ◽  
Evidence Based ◽  
Obstructive Pulmonary Disease ◽  
Copd Exacerbations ◽  
Different Types ◽  
Inflammatory Drugs ◽  
Long Acting

Exacerbations have significant impact on the morbidity and mortality of patients with chronic obstructive pulmonary disease. Most guidelines emphasise prevention of exacerbations by treatment with long-acting bronchodilators and/or anti-inflammatory drugs. Whereas most of this treatment is evidence-based, it is clear that patients differ regarding the nature of exacerbations and are likely to benefit differently from different types of treatment. In this short review, we wish to highlight this, suggest a first step in differentiating pharmacological exacerbation prevention and call for more studies in this area. Finally, we wish to highlight that there are perhaps easier ways of achieving similar success in exacerbation prevention using nonpharmacological tools.

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