Роль интерлейкина-27 при атеросклеротических сердечно-сосудистых заболеваниях

Алиева А.М., Теплова Н.В., Резник Е.В., Саракаева Л.Р., Рахаев А.М., Эльмурзаева Д.А., Аккиев М.И., Шаваева М.Я., Аккиева М.А., Никитин И.Г. Роль интерлейкина-27 при атеросклеротических сердечно-сосудистых заболеваниях. Consilium Medicum. 2023;25(10):668–673.
DOI: 10.26442/20751753.2023.10.202398

© ООО «КОНСИЛИУМ МЕДИКУМ», 2023 г.

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Alieva AM, Teplova NV, Reznik EV, Sarakaeva LR, Rahaev AM, Elmurzaeva DA, Akkiev MI, Shavaeva MYa, Akkieva MA, Nikitin IG. The role of interleukin-27 in atherosclerotic cardiovascular diseases: A review. Consilium Medicum. 2023;25(10):668–673. DOI: 10.26442/20751753.2023.10.202398

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Аннотация

Основной причиной развития многих сердечно-сосудистых заболеваний выступает атеросклероз. Атеросклеротический процесс, проявляющийся острыми сосудистыми катастрофами, такими как инфаркт миокарда и/или головного мозга, или хроническими ишемическими состояниями, такими как ишемическая болезнь сердца и цереброваскулярная болезнь, является, по сути, системным воспалительным процессом. Доказана весомая роль Т-клеток, макрофагов, нейтрофилов и цитокинов в данном патологическом процессе. Представленный литературный обзор указывает на потенциально важную диагностическую и прогностическую значимость оценки уровня интерлейкина-27. Ожидается, что дальнейшие научно-клинические исследования продемонстрируют возможности использования этого цитокина в качестве дополнительного лабораторного инструмента для диагностики, стратификации риска и прогнозирования сердечно-сосудистых катастроф у пациентов кардиологического профиля.

Ключевые слова: сердечно-сосудистые заболевания, биологические маркеры, атеросклероз, ишемическая болезнь сердца, цитокины, интерлейкин-27

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The main cause of many cardiovascular diseases is atherosclerosis. The atherosclerotic process, manifested by acute vascular accidents, such as myocardial and/or cerebral infarction, or chronic ischemic conditions, such as coronary heart disease and cerebrovascular disease, is essentially a systemic inflammatory process. The significant role of T-cells, macrophages, neutrophils and cytokines in this pathological process has been proven. The presented literature review indicates the potentially important diagnostic and prognostic value of the interleukin-27 assessment. It is expected that further scientific and clinical studies will demonstrate the possibility of using this cytokine as an additional laboratory tool for the diagnosis, risk stratification and prediction of cardiovascular events in patients with a cardiac profile.

Keywords: cardiovascular diseases, biological markers, atherosclerosis, coronary heart disease, cytokines, interleukin-27

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1. Shlyakhto EV, Zvartau NE, Villevalde SV, et al. Cardiovascular risk management system: prerequisites for developing, organization principles, target groups. Russian Journal of Cardiology. 2019;24(11):69-82 (in Russian). DOI:10.15829/1560-4071-2019-11-69-82
2. GBD 2015 Risk Factors Collaborators. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: A systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388(10053):1659-724. DOI:10.1016/S0140-6736(16)31679-8
3. Li H, Zou J, Yu XH, et al. Zinc finger E-box binding homeobox 1 and atherosclerosis: New insights and therapeutic potential. J Cell Physiol. 2021;236(6):4216-30. DOI:10.1002/jcp.30177
4. Fadeev GA, Fatykhov RG, Tsibulkin NA, et al. Inflammatory mechanisms in genesis of atherosclerosis. The Bulletin of Contemporary Clinical Medicine. 2020;13(6):62-7 (in Russian). DOI:10.20969/VSKM.2020.13(6).62-67
5. Jafarizade M, Kahe F, Sharfaei S, et al. The role of interleukin-27 in atherosclerosis: A contemporary review. Cardiology. 2021;146(4):517-30. DOI:10.1159/000515359
6. Witztum JL, Lichtman AH. The influence of innate and adaptive immune responses on atherosclerosis. Annu Rev Pathol. 2014;9:73-102. DOI:10.1146/annurev-pathol-020712-163936
7. Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med. 2011;17(11):1410-22. DOI:10.1038/nm.2538
8. Posadas-Sanchez R, Perez-Hernandez N, Rodriguez-Perez JM, et al. Interleukin-27 polymorphisms are associated with premature coronary artery disease and metabolic parameters in the Mexican population: the genetics of atherosclerotic disease (GEA) Mexican study. Oncotarget. 2017;8(38):64459-70. DOI:10.18632/oncotarget.16223
9. Pflanz S, Timans JC, Cheung J, et al. IL-27, a heterodimeric cytokine composed of EBI3 and p28 protein, induces proliferation of naive CD4+ T cells. Immunity. 2002;16(6):779-90. DOI:10.1016/s1074-7613(02)00324-2
10. Meka RR, Venkatesha SH, Dudics S, et al. IL-27-induced modulation of autoimmunity and its therapeutic potential. Autoimmun Rev. 2015;14(12):1131-41. DOI:10.1016/j.autrev.2015.08.001
11. Vargas-Alarcon G, Perez-Hernández N, Rodríguez-Perez JM, et al. Interleukin 27 polymorphisms, their association with insulin resistance and their contribution to subclinical atherosclerosis. The GEA Mexican study. Cytokine. 2019;114:32-7. DOI: 10.1016/j.cyto.2018.11.028
12. Caveney NA, Glassman CR, Jude KM, et al. Structure of the IL-27 quaternary receptor signaling complex. Elife. 2022;11:e78463. DOI:10.7554/eLife.78463
13. Han L, Chen Z, Yu K, et al. Interleukin 27 signaling in rheumatoid arthritis patients: Good or evil? Front Immunol. 2022;12:787252. DOI:10.3389/fimmu.2021.787252
14. Miteva K, Baptista D, Montecucco F, et al. Cardiotrophin-1 deficiency abrogates atherosclerosis progression. Sci Rep. 2020;10(1):5791. DOI:10.1038/s41598-020-62596-6
15. Chen Y, Zeng J, Zhang R, et al. Effect of interleukin-27 genetic variants on atrial fibrillation susceptibility. Genet Test Mol Biomarkers. 2017;21(2):97-101. DOI:10.1089/gtmb.2016.0219
16. Ye J, Wang Y, Wang Z, et al. Roles and mechanisms of interleukin-12 family members in cardiovascular diseases: Opportunities and challenges. Front Pharmacol. 2020;11:129. DOI:10.3389/fphar.2020.00129
17. Hibbert L, Pflanz S, De Waal Malefyt R, et al. IL-27 and IFN-alpha signal via Stat1 and Stat3 and induce T-bet and IL-12Rbeta2 in naive T cells. J Interferon Cytokine Res. 2003;23(9):513-22. DOI:10.1089/10799900360708632
18. Hunter CA, Kastelein R. Interleukin-27: Balancing protective and pathological immunity. Immunity. 2012;37(6):960-9. DOI:10.1016/j.immuni.2012.11.003
19. Moon SJ, Park JS, Heo YJ, et al. In vivo action of IL-27: Reciprocal regulation of Th17 and Treg cells in collagen-induced arthritis. Exp Mol Med. 2013;45(10):e46. DOI:10.1038/emm.2013.89
20. Kurdi M, Zgheib C, Booz GW. Recent developments on the crosstalk between STAT3 and inflammation in heart function and disease. Front Immunol. 2018;9:3029. DOI:10.3389/fimmu.2018.03029
21. Lucas S, Ghilardi N, Li J, de Sauvage FJ. IL-27 regulates IL-12 responsiveness of naive CD4+ T cells through Stat1-dependent and -independent mechanisms. Proc Natl Acad Sci U S A. 2003;100(25):15047-52. DOI:10.1073/pnas.2536517100
22. Yoshimoto T, Yoshimoto T, Yasuda K, et al. IL-27 suppresses Th2 cell development and Th2 cytokines production from polarized Th2 cells: a novel therapeutic way for Th2-mediated allergic inflammation. J Immunol. 2007;179(7):4415-23. DOI:10.4049/jimmunol.179.7.4415
23. Bosmann M, Ward PA. Modulation of inflammation by interleukin-27. J Leukoc Biol. 2013;94(6):1159–65. DOI:10.1189/jlb.0213107
24. Jones GW, Hill DG, Cardus A, Jones SA. IL-27: A double agent in the IL-6 family. Clin Exp Immunol. 2018;193(1):37-46. DOI:10.1111/cei.13116
25. Ma N, Fang Y, Xu R, et al. Ebi3 promotes T- and B-cell division and differentiation via STAT3. Mol Immunol. 2019;107:61-70. DOI:10.1016/j.molimm.2019.01.009
26. Dai L, Li Z, Tao Y, et al. Emerging roles of suppressor of cytokine signaling 3 in human cancers. Biomed Pharmacother. 2021;144:112262. DOI:10.1016/j.biopha.2021.112262
27. Owaki T, Asakawa M, Morishima N, et al. STAT3 is indispensable to IL-27-mediated cell proliferation but not to IL-27-induced Th1 differentiation and suppression of proinflammatory cytokine production. J Immunol. 2008;180(5):2903-11. DOI:10.4049/jimmunol.180.5.2903
28. Hirano T, Ishihara K, Hibi M. Roles of STAT3 in mediating the cell growth, differentiation and survival signals relayed through the IL-6 family of cytokine receptors. Oncogene. 2000;19(21):2548-56. DOI:10.1038/sj.onc.1203551
29. Qiu HN, Liu B, Liu W, Liu S. Interleukin-27 enhances TNF-α-mediated activation of human coronary artery endothelial cells. Mol Cell Biochem. 2016;411(1-2):1-10. DOI:10.1007/s11010-015-2563-3
30. Jafarzadeh A, Nemati M, Rezayati MT. Serum levels of interleukin (IL)-27 in patients with ischemic heart disease. Cytokine. 2011;56(2):153-6. DOI:10.1016/j.cyto.2011.06.014
31. Zhu L, Lin X, Chen M. LncRNA NEAT1 correlates with Th17 cells and proinflammatory cytokines, also reflects stenosis degree and cholesterol level in coronary heart disease patients. J Clin Lab Anal. 2022;36(6):e23975. DOI:10.1002/jcla.23975
32. Mease P, van den Bosch F. IL-23 and axial disease: Do they come together? Rheumatology (Oxford). 2021;60(Suppl. 4):iv28-iv33. DOI:10.1093/rheumatology/keab617
33. Baldrighi M, Mallat Z, Li X. NLRP3 inflammasome pathways in atherosclerosis. Atherosclerosis. 2017;267:127-38. DOI:10.1016/j.atherosclerosis.2017.10.027
34. Petes C, Wynick C, Guzzo C, et al. IL-27 enhances LPS-induced IL-1β in human monocytes and murine macrophages. J Leukoc Biol. 2017;102(1):83-94. DOI:10.1189/jlb.3A0316-098R
35. Gregersen I, Sandanger O, Askevold ET, et al. Interleukin 27 is increased in carotid atherosclerosis and promotes NLRP3 inflammasome activation. PLoS One. 2017;12(11):e0188387. DOI:10.1371/journal.pone.0188387
36. Guzzo C, Ayer A, Basta S, et al. IL-27 enhances LPS-induced proinflammatory cytokine production via upregulation of TLR4 expression and signaling in human monocytes. J Immunol. 2012;188(2):864-73. DOI:10.4049/jimmunol.1101912
37. Jin W, Zhao Y, Yan W, et al. Elevated circulating interleukin-27 in patients with coronary artery disease is associated with dendritic cells, oxidized low-density lipoprotein, and severity of coronary artery stenosis. Mediators Inflamm. 2012;2012:506283. DOI:10.1155/2012/506283
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Авторы

А.М. Алиева*¹, Н.В. Теплова¹, Е.В. Резник¹, Л.Р. Саракаева², А.М. Рахаев³, Д.А. Эльмурзаева³, М.И. Аккиев³, М.Я. Шаваева³, М.А. Аккиева⁴, И.Г. Никитин¹

¹ФГАОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И. Пирогова» Минздрава России, Москва, Россия;
²ФГБУ «Национальный медицинский исследовательский центр им. В.А. Алмазова» Минздрава России, Санкт-Петербург, Россия;
³ФГБОУ ВО «Кабардино-Балкарский государственный университет им. Х.М. Бербекова» Минобрнауки России, Нальчик, Россия;
⁴ГБУЗ «Центр аллергологии и иммунологии» Минздрава Кабардино-Балкарской Республики, Нальчик, Россия
*amisha_alieva@mail.ru

________________________________________________

Amina M. Alieva*¹, Natalya V. Teplova¹, Elena V. Reznik¹, Leyla R. Sarakaeva², Alik M. Rahaev³, Dzhannet A. Elmurzaeva³, Makhty I. Akkiev³, Madina Ya. Shavaeva³, Maryana A. Akkieva⁴, Igor G. Nikitin¹

¹Pirogov Russian National Research Medical University, Moscow, Russia;
²Almazov National Medical Research Center, Saint Petersburg, Russia;
³Berbekov Kabardino-Balkarian State University, Nalchik, Russia;
⁴Center of Allergology and Immunology, Nalchik, Russia
*amisha_alieva@mail.ru

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