Peculiarities  of  Course  of  Chronic  Obstructive  Pulmonary  Disease  With  Underlying  Metabolic  Syndrome

Budnevsky, A. V.; Ovsyannikov, Evgeniy; Maltseva, Yu.N.; Polyakova, N.V.; Shkatova, Ya.S.

doi:10.23888/hmj202082164-171

Cited by 3 publications

(1 citation statement)

References 7 publications

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“…Рентгенологическая картина осложненной метаболическим синдромом ХОБЛ характеризуется усилением легочного рисунка; при электрокардиографии в 3 раза чаще, чем у больных с изолированной ХОБЛ, регистрируются признаки перегрузки правых отделов сердца. Установлено, что ишемическая болезнь сердца у больных ХОБЛ на фоне метаболического синдрома формируется в среднем на 9 лет раньше, чем при изолированной ХОБЛ; чаще развиваются нарушения сердечного автоматизма и проводимости; острые нарушения мозгового кровообращения у пациентов с сочетанной патологией регистрируются на 12,3% чаще, чем при отсутствии метаболических расстройств [12,[44][45][46][47][48][49][50][51].…”

Section: научный обзорunclassified

Etiopathogenetic parallels and unresolved issues of pathogenesis of comorbidity COPD and metabolic syndrome (review)

et al. 2020

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The review analyzes the etiological and pathogenetic factors (including immunopathogenesis factors) of chronic obstructive pulmonary disease (COPD) and metabolic syndrome (MS), cites data on clinical and pathogenetic characteristics of combined pathology, emphasizes the commonality of risk factors and individual links of pathogenesis in syntropy.The clinical and pathogenetic features of the comorbidity of COPD and MS are closely related to the severity of chronic “metabolic” inflammation induced by elements of adipose tissue. Functional and biochemical disorders recorded in metabolic syndrome (insulin resistance, hyperglycemia, dyslipidemia) are considered as factors contributing to dysfunction of the components of innate and adaptive immunity.The review formulates a number of unresolved issues of the pathogenesis of comorbid pathology, the study of which is necessary to search for the mutual aggravating effect of COPD and MS mechanisms. In view of the clinical and laboratory metabolic syndrome equivalents variety, the authors emphasize the relevance of future studies of the pathogenetic features of chronic inflammation associated with the comorbidity of the main components of metabolic syndrome and COPD, to develop effective methods of prevention and pathogenetic therapy of comorbid pathology.

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Section: научный обзорunclassified

Etiopathogenetic parallels and unresolved issues of pathogenesis of comorbidity COPD and metabolic syndrome (review)

et al. 2020

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The role of cytokines in the development of systemic inflammation in chronic obstructive pulmonary disease and obesity

et al. 2023

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Patients with chronic obstructive pulmonary disease (COPD) are characterized by a variety of comorbid conditions, including both somatic (arterial hypertension, atherosclerosis, coronary heart disease, bronchial asthma, malignant neoplasms, diabetes mellitus, obesity, etc.) and mental (depressive disorders, suicide attempts). Against the background of various chronic diseases of the respiratory system, endocrine, metabolic disorders, the risks of exacerbations of COPD increase.The leading unifying mechanism of these conditions is systemic subclinical inflammation. Its excessive activity leads to the loss of the physiological functions of inflammation, which is accompanied by an imbalance in the endocrine system and the release of high concentrations of hormones and neurotransmitters. The result of this response is the uncoupling of cytokine mechanisms, which leads to an imbalance in the system of pro- and anti-inflammatory cytokines.The article describes the role of the pro-inflammatory chemokine IL-8 (interleukin 8), which is responsible for the migration of neutrophils to the site of inflammation. This is how the neutrophilic type of inflammation is formed. IL-4 and IL-10 are considered, which occupy a leading position in the formation of CD4+ type of immunoreactivity, which is observed in bronchial asthma. Attention is focused on the significance of IL-6, because it is an integral component of local and systemic inflammation. An increase in its concentration and, as a result, a potential risk of damage to the respiratory epithelium is the remodeling of the bronchial tree, resulting in a decrease in the elasticity of the epithelium of the respiratory tract. This mechanism leads to the formation of pulmonary emphysema and further potentiation of pathophysiological processes in patients with COPD.Since IL-6 is a cytokine with anti-inflammatory properties, its molecular activity is achieved by interacting with a special receptor complex consisting of two subunits: IL-6R and gp130. The former mediates IL-6 binding, while the latter triggers the JAK/STAT or MAPK signaling cascade pathways. The result of the reaction of IL-6 with the effector cell directly depends on the type of signaling.The paper describes three mechanisms of signal transduction into the target cell: classical, cluster, and transsignaling.Thus, by studying the role of cytokines in the systemic inflammatory response, we have shown the cross-talk between adipose tissue and the lungs in obesity, highlighting the main inflammatory mediators, which may indicate new therapeutic targets for preventing pulmonary dysfunction.

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Analysis of Influence of Cigarette Smoke on Signaling Pathways of Innate Immune System in Monocytes of Peripheral Blood

Kotlyarov,

Suchkov,

Uryas'yev

et al. 2023

I.P. Pavlov Russian Medical Biological Herald

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INTRODUCTION: Tobacco smoking is an important medical problem since it has a significant impact on the development and progression of chronic obstructive pulmonary disease (COPD). The components of tobacco smoke can initiate and support local and systemic inflammation with participation of monocytes and macrophages. AIM: To study molecular mechanisms associated with the impact of cigarette smoke on signaling pathways of the innate immune system in monocytes of peripheral blood. MATERIALS AND METHODS: The methods of in silico analysis was used to identify genes associated with the impact of tobacco smoke. On the basis of the data obtained, a cellular model of inflammation was created in vitro using tobacco smoke extract and monocytes of peripheral blood isolated by immunomagnetic separation. An enzyme-linked immunoassay (ELISA) kit was used to measure the concentration of tumor necrosis factor- (TNF-), interleukin-1 (IL-1) in cell supernatants, and of Toll-like receptor 4 (TLR4), ATP-binding cassette A1 (ABCA1) in homogenates of cell membranes of native monocytes and monocytes exposed to 4% tobacco smoke extract. These data were compared with the levels of TNF-, IL-1, TLR4 and ABCA1 in monocytes of peripheral blood of patients with COPD with frequent exacerbation phenotype and with obliterating atherosclerosis of lower limb arteries (OALLA). For statistical processing and visualization of the data, MedCalc 20.1.4 and R (version 4.2.2) software was used. RESULTS: Tobacco smoke influences TLR4, TNF- signaling pathways and lipid metabolism. Cigarette smoke extract enhanced the expression of proinflammatory cytokines TNF- and IL-1 in cell supernatants, increased the level of TLR4 and decreased that of ABCA1 in plasmolemma of monocytes of peripheral blood. In patients with COPD with frequent exacerbation phenotype and with OALLA, there were shown increase in the levels of proinflammatory TNF- and IL-1 cytokines in cell supernatants, increase in the level of TLR4 and reduction of the level of ABCA1 in plasmolemma of monocytes of peripheral blood compared to native monocytes of healthy individuals. CONCLUSION: Cigarette smoke enhances the production of proinflammatory TNF- and IL-1 cytokines, increases the levels of TLR4 protein and reduces the amount of ABCA1 transporter in membranes of monocytes of peripheral blood. This may partially explain the cause of the influence of cigarette smoke on development of the pulmonary and cardiovascular diseases. COPD with frequent exacerbation phenotype and OALLA are characterized by enhancement of inflammation with participation of monocytes.

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Peculiarities of Course of Chronic Obstructive Pulmonary Disease With Underlying Metabolic Syndrome

Cited by 3 publications

References 7 publications

Etiopathogenetic parallels and unresolved issues of pathogenesis of comorbidity COPD and metabolic syndrome (review)

Etiopathogenetic parallels and unresolved issues of pathogenesis of comorbidity COPD and metabolic syndrome (review)

The role of cytokines in the development of systemic inflammation in chronic obstructive pulmonary disease and obesity

Analysis of Influence of Cigarette Smoke on Signaling Pathways of Innate Immune System in Monocytes of Peripheral Blood

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