Interleukin-8 is able to promote pro-inflammatory activity of human monocytes (macrophages)

Meniailo, Maksim Evgenievich; Малащенко, В. В.; Shmarov, V.A.; Газатова, Н. Д.; Melashchenko, Olga Borisovna; Goncharov, A. G.; Селедцова, Г. В.; Селедцов, В. И.

doi:10.23868/201805007

Cited by 5 publications

(7 citation statements)

References 23 publications

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“…Интерлейкин 8 (IL-8/CXCL8) представляет собой мощный провоспалительный цитокин, взаимодействующий с рецепторами IL-8α (IL-8RA, CXCR1), IL-8β (IL-8RB, CXCR2) и стимулирующий активацию, миграцию нейтрофилов, моноцитов и лимфоцитов из периферической крови в очаг воспаления [1,2]. Он играет решающую роль в инициации воспалительного ответа на патохимической стадии развития бронхиальной астмы (БА), ассоциируясь с патогенетическими элементами болезни [1] и полиморфизмами гена IL-8RA.…”

Section: оригинальные исследования Original Researchunclassified

“…Интеграция IL-8 с IL-1, гранулоцитарно-макрофагальным колониестимулирующим фактором (GM-СSF), фактором некроза опухоли альфа (TNFα) и другими провоспалительными медиаторами составляет цитокиновый фон, активирующий функции нейтрофилов [4,5], в результате чего синтезируются и продуцируются нейтрофилокины (GM-СSF, TNFα, IL-1β, IL-6, IL-8), участвующие в кооперативном взаимодействии фагоцитов и действующие паракринно на макрофаги, аутокринно -на нейтрофилы [6]. Поскольку ведущая роль продуцентов IL-8 в иммунной системе отводится макрофагам, доказано непосредственное участие IL-8 в аутокринной регуляции функциональной активности этих клеток [2].…”

Section: оригинальные исследования Original Researchunclassified

“…В 2010 году Номенклатурным комитетом Международного союза иммунологических обществ среди мононуклеарных фагоцитов -моноцитов и макрофаговбыло выделено три популяции: классические (CD14 + CD16 -), неклассические (CD14 ++ CD16 + ) и переходные (CD14 + CD16 ++ ), с объединением в некоторых случаях неклассической и переходной в одну популяцию (CD14 + CD16 + ) [2,7]. Аутокринная стимуляция интерлейкином 8 воспалительной активности макрофагов (М), заключающаяся в поддержании классической CD14 + CD16популяции макрофагальных предшественников и поляризации клеток в классический М1-фенотип [2], является одним из патогенетических звеньев неаллергической астмы. В иммунном ответе больных БА М1 макрофаги эффективно активируют клетки Т-хелперы первого типа (Тh1), секретируя большой спектр цитокинов, а также NO и активные формы кислорода (reactive oxygen species (ROS)) [8][9][10][11][12][13].…”

Section: оригинальные исследования Original Researchunclassified

“…Ранее была показана высокая подверженность макрофагов к дифференцировке в классически и альтернативно активированные формы (М1 и М2) благодаря цитокиновому/хемокиновому микроокружению. Способность генерироваться в М1 макрофаги происходит под воздействием Тh1 цитокинов и микробных продуктов [2]. Помимо IL-8, мощными индукторами поляризации клеток в фенотип М1 выступают липополисахарид (LPS), интерферон гамма (IFN-γ), GM-CSF, IL-17, IL-32 [10,13].…”

Section: результаты исследования и их обсуждениеunclassified

“…Согласно данным, полученным in vitro, IL-8, заметно уменьшая содержание CD16 + (FcγRIII) клеток среди LPS-активированных макрофагов, увеличивает количество макрофагов, экспрессирующих рецептор к IFN-γ (CD119) и снижает количество клеток, несущих рецептор к IL-4 (CD124) [2]. IFN-γ, поляризующий иммунный ответ по Тh1типу и активацию М1 макрофагов [8][9][10][11][12], индуцируя NADPH-зависимую фагоцитарную оксидазу, праймирует респираторный взрыв в макрофагах, стимулирует синтез NO, снижает запасы триптофана и увеличивает продукцию ферментов лизосом [20].…”

Section: результаты исследования и их обсуждениеunclassified

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Interleukin 8 and bronchial phagocytes in patients with non-allergic asthma and diverse respiratory responses to cold stimulus

Pirogov,

Prikhodko,

Perelman

2024

Bûlletenʹ fiziologii i patologii dyhaniâ

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Introduction. The role of phagocytes, regulated by interleukin 8 (IL-8), in the formation of the bronchial response to environmental stimuli in patients with asthma is not well understood.Aim. To study the functional activity of IL-8 and the pool of phagocytic cells in the inflammatory pattern of the bronchi in patients with non-allergic asthma during inhalation exposure to cold air.Materials and methods. In 129 patients with mild to moderate asthma, the content of IL-8 and the cellular composition of sputum before and after the bronchoprovocation test with isocapnic hyperventilation with cold air (-20°C) (IHCA) were analyzed.Results. Based on the results of the IHCA by the assessment of changes in FEV1 (Δ,%), 54 patients (1st group) were verified with cold airway hyperresponsiveness (CAHR), the comparison group consisted of asthma patients (2nd group, n=75) who did not respond to the trigger (ΔFEV1 = -18.9±1.2 and -3.3±0.4%; p<0.0001, respectively). The content of neutrophils in sputum before provocation was 41.1±2.2% and 34.5±2.2% (p><0.05), macrophages – 36.2±2.7% and 43.1±2.5% (p> ˂ 0.0001, respectively). The content of neutrophils in sputum before provocation was 41.1±2.2% and 34.5±2.2% (p ˂ 0.05), macrophages – 36.2±2.7% and 43.1±2.5% (p>0.05), respectively. In response to the IHCA in the 1st group, the number of neutrophils increased to 48.2±2.0% (p ˂ 0.05), macrophages decreased to 28.7±2.1% (p ˂ 0.01), and the level of IL-8 increased from 12838±2328 to 17412±2980 pg/mL (p ˂ 0.05). In the 2nd group, the concentration of IL-8 before the IHCA was 14639±2691 pg/mL, after the test 10545±1746 pg/mL (p>0.05); the number of neutrophils after the test 40.0±2.3% (p>0.05); macrophages – 35.8±2.0% (p ˂ 0.01).Conclusion. In asthma patients with CAHR, the inflammatory pattern of the bronchi in response to the cold trigger shows enhanced IL-8 activity and more pronounced changes in the content of phagocytes, mobilized with the involvement of this cytokine.

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Section: оригинальные исследования Original Researchunclassified

Section: результаты исследования и их обсуждениеunclassified

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Interleukin 8 and bronchial phagocytes in patients with non-allergic asthma and diverse respiratory responses to cold stimulus

Pirogov,

Prikhodko,

Perelman

2024

Bûlletenʹ fiziologii i patologii dyhaniâ

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Dynamics of cytokine status of blood serum in adolescents with varicocele

2023

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Varicocele is a varicose dilation of pampiniform plexus veins in testicular gland, considered a special case of phlebopathy. With varicocele, there is impaired venous outflow via the left renal vein from the veins of testicular pampiniform plexus. Increased hydrostatic pressure leads to failure of the wall tone of the testicular vein, valvular venous insufficiency with dilation of the local venous system. Vasodilation requires integrity of endothelial layer, and its damage resulting from hydrodynamic stress is a trigger for development of an inflammatory response and production of cytokines. Pro-inflammatory cytokines have a pronounced damaging effect on endothelial cells, leading to endothelial dysfunction and chronic inflammation. Angiogenesis is an important characteristic of inflammatory disorders. Both inflammation and its controlling mechanisms employ many common factors, including IL-1β, IL-6, IL-8, TNFα. The purposes of our study were: to determine the dynamics of the pro- and anti-inflammatory cytokine levels, and VEGF contents in blood serum of adolescents with left-sided varicocele in order to assess the severity of inflammatory reaction of the vessels in the pampiniform plexus as well as prognosis of angiogenesis and remodeling of the testicular veins. We examined 100 adolescents with left-sided varicocele II-III degree and 30 adolescents without varicocele, who made up the comparison group. All adolescents (14 to 17 years old) underwent determination of IL-1β, IL-6, IL-8, TNFα, IL-4, IL-10, VEGF levels in blood serum at a frequency of 1 year, depending on the degree of varicocele, terms after varicocelectomy.Statistically higher levels of pro-inflammatory cytokines were found over different age periods in adolescents with varicocele, as well as increased levels of anti-inflammatory cytokines, which may suggest an inflammatory process in testicular veins associated with varicocele. Higher levels of pro-inflammatory cytokines were found in patients with grade III varicocele compared with patients with grade II condition, but without statistically significant differences. In adolescents prior to varicocelectomy, significantly higher levels of cytokines were determined, which persisted over the postoperative period. Based on these results, one may assume that, in phlebopathy, the inflammatory process persists until surgical correction, and adaptation to the changed blood flow after surgery does not take time. VEGF values remain approximately similar over the observation period, and, probably, the changes of the vessel walls occur due to inflammatory process, and not to activation of angiogenesisIn varicocele disorder, an inflammatory status is observed in the altered testicular venous plexus, being more pronounced in grade III varicocele and affected by subsequent surgical correction.

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Outcomes of sepsis: a new look at old problems

et al. 2022

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Infections represent a common health problem in people at any age. Usually, a local reaction develops in response to the infection, and intensive treatment is not required. However, sometimes the response to infection is inadequate and may lead to organ dysfunction; such condition is defined as septic state. The pathophysiology of sepsis is multifactorial, and the immune system is directly involved in development of pathological processes accompanying septic conditions. Dysregulatory disorders in sepsis may be observed, in particular, those affecting immune system and, immediately, innate immunity, which presents the first line of immune defense. Currently, neutrophilic granulocytes are considered important players in development and maintenance of inflammatory processes, which is due to their ability to produce various inflammatory mediators. At the same time, at different stages of pathogenesis, immune factors and mechanisms act both as a generating factors and effectors of damage reactions, as well as the main components of the defense responses. Uncontrolled release of endogenous inflammatory mediators induced by microorganisms, and lack of damagelimiting mechanisms mutually synergize when promoting the organ dysfunction. Hence, dysfunction of the immune system may develop and deepen upon any inappropriate strategy of response to distinct infectious pathogen. The aim of our study was to assess the spectrum of microorganisms, levels of neutrophilic extracellular traps (NVL), PAD4, IL-6, IL-8 and their correlations in the patients with sepsis and septic shock, depending on the outcome of the disease. The study included 44 patients with sepsis and septic shock, and 20 apparently healthy donors. Peripheral blood samples were taken from the ulnar vein serially in dynamics, from the moment of diagnosis to clinical outcome. Microbiological and immunological studies have been carried out. The obtained data were processed with “SPSS Statistic 23.0” software. Development of septic conditions was found to be accompanied by a significant changes in the levels of studied immunological parameters (NLV, IL-6, IL-8 and PAD4). Toxicity of lysosomal enzymes and oxygen metabolites present in neutrophilic extracellular traps leads to endothelial damage, appearance of focal intravascular inflammation, which, along with damaging effects of microorganisms and their toxins, leads to development of organ failure and onset. High burden of these factors is most likely to cause lethal outcomes.

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Interleukin-8 is able to promote pro-inflammatory activity of human monocytes (macrophages)

Cited by 5 publications

References 23 publications

Interleukin 8 and bronchial phagocytes in patients with non-allergic asthma and diverse respiratory responses to cold stimulus

Interleukin 8 and bronchial phagocytes in patients with non-allergic asthma and diverse respiratory responses to cold stimulus

Dynamics of cytokine status of blood serum in adolescents with varicocele

Outcomes of sepsis: a new look at old problems

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