psychiatryПСИХИАТРИЯPsychiatry (Moscow) (Psikhiatriya)1683-83192618-6667FSBSI “The Mental Health Research Centre”; LLC «Publisher «MIA»10.30629/2618-6667-2020-18-4-81-92psychiatry-551Research ArticleНАУЧНЫЕ ОБЗОРЫSCIENTIFIC REVIEWSКлеточно-молекулярные механизмы участия провоспалительных моноцитов в патогенезе психических расстройств. Часть 2Сellular and Molecular Mechanisms of Proinflammatory Monocytes Participation in the Pathogenesis of Mental Disorders. Part 2https://orcid.org/0000-0002-0218-833XВасильеваЕ. Ф.VasilyevaE. F.

Васильева Елена Федоровна, кандидат биологических наук, старший научный сотрудник, лабораториябиохимии

Москва

Elena F. Vasilyeva, PhD, Cand. of Sci. (Biol.), Senior Researcher, laboratory of Biochemistry

Moscow

el_vasiliyeva@mail.ruhttps://orcid.org/0000-0003-1269-679XБрусовО. С.BrusovO. S.

Брусов Олег Сергеевич, кандидат биологических наук, заведующий лабораторией биохимии

Москва

Oleg S. Brusov, PhD, Cand. of Sci. (Biol.), Head of Biochemistry laboratory

Moscow

oleg.brusow@yandex.ruФГБНУ «Научный центр психического здоровья»РоссияFSBSI “Mental Health Research Centre”Russian Federation2020151220201848192Copyright © Васильева Е.Ф., Брусов О.С., 20202020Васильева Е.Ф., Брусов О.С.Vasilyeva E.F., Brusov O.S.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.journalpsychiatry.com/jour/article/view/551Обоснование

Обоснование: в конце прошлого века была сформулирована макрофагально-Т-лимфоцитарная теория развития психических расстройств, в которой определялась важная роль моноцитов/макрофагов и продуцируемых ими цитокинов в патогенезе шизофрении, биполярного аффективного расстройства (БАР) и депрессии. В первой части нашего обзора проанализированы механизмы клеточно-молекулярных взаимодействий активированных моноцитов/макрофагов, синтезирующих провоспалительные рецепторы CD16, с клетками эндотелия, тромбоцитами, с клетками микроглии в патогенезе системных иммунных воспалений, к которым относят диабет, атеросклероз, онкологические, нейродегенеративные и другие заболевания. Известно, что иммунные клетки в результате нарушения целостности гематоэнцефалического барьера (ГЭБ) могут мигрировать в ЦНС, активировать микроглию и вызывать развитие нейровоспаления у больных.

Цель

Цель: провести анализ и обобщить результаты основных научных публикаций по исследованию роли клеточно-молекулярных механизмов активации моноцитарно-макрофагального звена иммунитета в патогенезе шизофрении, БАР и депрессии.

Материал и методы

Материал и методы: по ключевым словам «провоспалительные моноциты, цитокины, хемокины, молекулы клеточной адгезии, микроглия, психические расстройства, нейровоспаление» проведен поиск результатов отечественных и зарубежных исследований, опубликованных за последние 20 лет в базах данным PubMed, eLIBRARY.RU, Science direct и EMBASE.

Заключение

Заключение: в настоящем обзоре проанализированы современные данные литературы, которые свидетельствуют об увеличении количества активных циркулирующих моноцитов/ макрофагов и повышенном уровне синтезируемых ими провоспалительных цитокинов, хемокинов и рецепторов к ним у больных шизофренией, БАР и депрессией, на основании чего эти заболевания связывают с системным иммунным воспалением. Приведены результаты исследований клеточно-молекулярных механизмов взаимодействия провоспалительных моноцитов/макрофагов с клетками микроглии, инициирующих нейровоспаление в ЦНС и приводящих к дестабилизации функции мозга и развитию психических расстройств. Показана связь высоких уровней провоспалительных цитокинов у больных с психическими расстройствами с соматической коморбидностью, в том числе с метаболическим синдромом, с диабетом, атеросклерозом и другими системными заболеваниями. Представленный обзор данных литературы расширяет представления о клеточно-молекулярных аспектах активации моноцитарно-макрофагального звена иммунитета в развитии нейровоспаления и когнитивного снижения в патогенезе психических заболеваний, а также помогает в поисках информативных биомаркеров положительного ответа на лечение этих расстройств и новых подходов к терапии больных, основанных на комплексном применении психотропных и противовоспалительных препаратов.

Introduction

Introduction: at the end of the last century, the macrophage-T-lymphocyte theory of the development of mental disorders was formulated. It underlines the important role of monocytes/macrophages and cytokines produced by them in the pathogenesis of schizophrenia, bipolar affective disorder (BAD) and depression. The first part of our review is dedicated to the analysis of the mechanisms of cellular and molecular interactions of activated monocytes/macrophages synthesizing proinflammatory CD16 receptors with endothelial cells, platelets, and microglia cells in the pathogenesis of systemic immune inflammation, including CNS as a result of violation of the integrity of the blood-brain barrier (BBB), activate microglia and cause the development of neuroinflammation in patients.

The aim of work

The aim of work: to analyze and summarize the results of the main scientific publications for the role of cell-molecular mechanisms of the monocyte-macrophage immunity link activation in the pathogenesis of schizophrenia, BAD and depression. Material and methods: keywords “proinflammatory monocytes, cytokines, chemokines, molecules of cell adhesion, microglia, neuroinflammation, mental disorders” were used to search for data published over the past 20 years in domestic and foreign studies in PubMed, eLIBRARY, Science direct and EMBASE.

Conclusion

Conclusion: the present review is dedicated to the analysis of the latest research data concerning an increase in the number of active circulating monocytes/macrophages and an increased level of proinflammatory cytokines, chemokines and receptors for them produced by monocytes in patients with schizophrenia, BAD and depression, what allows to associate these disorders with systemic immune inflammation. The data reasearches on cellular and molecular mechanisms of proinflammatory monocytes/macrophages interaction with microglia cells that initiate neuroinflammation in the CNS and lead to destabilization of brain function and the development of psychotic disorders are presented. The association of high levels of proinflammatory cytokines with somatic comorbidity, including metabolic syndrome, diabetes, atherosclerosis and other systemic diseases is shown in patients with mental disorders.

Findings

Findings: the presented review of the research data allows us to better understand the cellular and molecular aspects of activation of the monocyte-macrophage immunity link in the development of neuroinflammation and cognitive decline in the pathogenesis of mental disorders, as well as helps in the search for informative biomarkers of the positive treatment of these disorders and the new approaches in the treatment of patients, based on the complex use of psychotropic and anti-inflammatory drugs.

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The authors declare that there are no conflicts of interest present.