Features of the content of pro-inflammatory cytokins in chronic heart failure

Authors

  • Naira Lipkan Nizhyn Gogol State University, National Scientific Center "Institute of Cardiology, Clinical and Regenerative Medicine named after Academician M.D. Strazheska of the National Academy of Medical Sciences of Ukraine"
  • Olena Kuchmenko Nizhyn Gogol State University

DOI:

https://doi.org/10.29038/NCBio.23.1-12

Keywords:

cytokines, immune cells, immune-inflammatory reaction, ischemic heart disease, arterial hypertension, chronic heart failure

Abstract

Various endogenous mechanisms are involved in the development and progression of chronic heart failure (CHF). The aim of the study was to study the content of pro-inflammatory cytokines, namely tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), in patients with CHF. The study included 149 patients with CHF, aged 18 to 75 years, who were receiving inpatient treatment in the heart failure department of the National Center for Cardiology "Institute of Cardiology named after Acad. M.D. Strazheska" of the National Academy of Sciences of Ukraine during 2020-2022. TNF-α and IL-6 were determined in blood serum and supernatants by the enzyme-linked immunosorbent assay method. An increase (p ≤ 0.05) in the levels of TNF-α and IL-6 in the blood serum of patients with CHF was demonstrated. A higher level of studied cytokines was observed in patients with atrial fibrillation compared to patients with sinus rhythm. The levels of TNF-α and IL-6 increased with increasing of functional class. The highest levels were observed in patients with left ventricular ejection fraction ≤ 25% and 26-35% compared to the group of patients with left ventricular ejection fraction ≥ 36%. Also, the level of these pro-inflammatory cytokines increased with the age of the disease. Depending on the diagnosis, the highest level of TNF-α was observed in patients with dilated cardiomyopathy, and the lowest (at the control level) in patients with coronary heart disease without hypertensive disease. At the same time, the levels of IL-6 in the blood of these patients are opposite - the lowest level is observed in patients with dilated cardiomyopathy, and the highest level is observed in patients with coronary heart disease without hypertensive disease. Also, an increase (p ≤ 0.05) in the cytokine-producing capacity of the peripheral blood mononuclear cells of patients with CHF, both spontaneous and induced, was shown. At the same time, changes in the values of the studied indicators in different subgroups were similar to changes in the content of cytokines in the blood of patients. It was established that the immune-inflammatory activation of immunocompetent cells was enhanced in all patients with CHF.

References

De Angelis, E.; Pecoraro, M.; Rusciano, M. R.; Ciccarelli, M.; Popolo, A. Cross-Talk between Neurohormonal Pathways and the Immune System in Heart Failure: A Review of the Literature. Int J Mol Sci. 2019, 20 (7), p 1698.

Halade, G. V.; Lee, D. H. Inflammation and resolution signaling in cardiac repair and heart failure. EBioMedicine. 2022, 79, p 103992.

Dutka, M.; Bobiński, R.; Ulman-Włodarz, I.; Hajduga, M.; Bujok, J.; Pająk, C.; Ćwiertnia, M. Various aspects of inflammation in heart failure. Heart Fail Rev. 2020, 25 (3), pp 537–548.

Zhang, Y.; Bauersachs, J.; Langer, H. F. Immune mechanisms in heart failure. Eur J Heart Fail. 2017, 19 (11), pp 1379–1389.

Hanna, A.; Frangogiannis, N. G. Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure. Cardiovasc Drugs Ther. 2020, 34 (6), pp 849–863.

Chirinos, J.A.; Orlenko, A.; Zhao, L.; Basso, M. D.; Cvijic, M. E.; Li, Z.; Spires, T. E.; Yarde, M.; Wang, Z.; Seiffert, D. A.; Prenner, S.; Zamani, P.; Bhattacharya, P.; Kumar, A.; Margulies, K. B.; Car, B. D.; Gordon, D. A.; Moore, J. H.; Cappola, T. P. Multiple Plasma Biomarkers for Risk Stratification in Patients With Heart Failure and Preserved Ejection Fraction. J Am Coll Cardiol. 2020, 75 (11), pp 1281–1295.

Cupido, A. J.; Asselbergs, F. W.; Natarajan, P.; CHARGE Inflammation Working Group; Ridker, P. M.; Hovingh, G. K.; Schmidt, A. F. Dissecting the IL-6 pathway in cardiometabolic disease: A Mendelian randomization study on both IL6 and IL6R. Br J Clin Pharmacol. 2022, 88 (6), pp 2875–2884.

Schumacher, S. M.; Naga Prasad, S. V. Tumor Necrosis Factor-α in Heart Failure: an Updated Review. Curr Cardiol Rep. 2018, 20 (11), p 117.

Rolski, F.; Błyszczuk, P. Complexity of TNF-α Signaling in Heart Disease. J Clin Med. 2020, 9 (10), p 3267.

Dittrich, G. M.; Heineke, J. TNF-α signaling: TACE inhibition to put out the burning heart. PLoS Biol. 2020, 18 (12), p e3001037.

Lipkan, N. G.; Kuchmenko, O. B.; Mkhitaryan, L. S. Aktyvnist indutsybelnoi NO-syntazy ta vmist tsytrulinu v syrovattsi krovi yak markery imunozapalnoi aktyvatsii ta oksydatyvnoho stresu pry khronichnii sertsevii nedostatnosti [Inducible NO-synthase activity and citrulline content in blood serum as markers of immune-inflammatory activation and oxidative stress in chronic heart failure]. Visnyk medychnykh i biolohichnykh doslidzhen. 2021, 4 (10), 46–52. (in Ukrainian)

Markousis-Mavrogenis, G.; Tromp, J.; Ouwerkerk, W.; Devalaraja, M.; Anker, S. D.; Cleland, J. G.; Dickstein, K.; Filippatos, G. S.; van der Harst, P.; Lang, C. C.; Metra, M.; Ng, L. L.; Ponikowski, P.; Samani, N. J.; Zannad, F.; Zwinderman, A. H.; Hillege, H. L.; van Veldhuisen, D. J.; Kakkar, R.; Voors, A. A.; van der Meer, P. The clinical significance of interleukin-6 in heart failure: results from the BIOSTAT-CHF study. Eur J Heart Fail. 2019, 21 (8), pp 965–973.

Perez, A. L.; Grodin, J. L.; Chaikijurajai, T.; Wu, Y.; Hernandez, A. F.; Butler, J.; Metra, M.; Felker, G. M.; Voors, A. A.; McMurray, J. J.; Armstrong, P. W.; O'Connor, C.; Starling, R. C.; Tang, W. H. W. Interleukin-6 and Outcomes in Acute Heart Failure: An ASCEND-HF Substudy. J Card Fail. 2021, 27 (6), pp 670–676.

Published

2023-06-30

Issue

Section

Human and Animal Physiology

How to Cite

Features of the content of pro-inflammatory cytokins in chronic heart failure. (2023). Notes in Current Biology, 1 (5), 82-88. https://doi.org/10.29038/NCBio.23.1-12