Comparative immunohistochemical and morphometric research of interleukin-17 in various atherosclerotic lesions in human

Cover Page


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

The aim of the artical — to investigate cellular and tissue localization of IL-17 in various atherosclerotic lesions of arteries of human and on the basis of the obtained data to make a hypothesis of a possible role of Th17 of cells in destabilization of an atherosclerotic plaque.

Material and methods. On autopsy material by means of histologic, immunohistochemical and morphometric research techniques aorta segments, the coronary arteries and a. basilaris with various types of atherosclerotic lesions (43 samples of tissue) were studied. In samples of tissue studied the endothelial and mononuclear cells expressing IL-17.

Results. It is shown that endothelial cells of an intima are capable to produce IL-17 in all types of atherosclerotic plaques. Increase in number of the mononuclear cells expressing IL-17 in an intima of arteries was at the same time revealed. It is shown that the maximum number of the cells expressing IL-17 was found in an intima of an unstable atherosclerotic plaque, it is especially frequent around a rupture of its cap. What can demonstrate pro-inflammatory action of Th17-cells and IL-17 expressed by them and significant effect them on formation of unstable atherosclerotic lesions.

Conclusion. On the basis of the obtained data for the first time it was succeeded to make a hypothesis of a possible role of Th-17 of cells in destabilization of an atherosclerotic plaque.

Full Text

Restricted Access

About the authors

Peter V. Pigarevsky

Institute of Experimental Medicine

Author for correspondence.
Email: pigarevsky@mail.ru
ORCID iD: 0000-0002-5906-6771
SPIN-code: 8636-4271

PhD (Biology), Head, Department of General Morphology

Russian Federation, Saint Petersburg

Vlada A. Snegova

Institute of Experimental Medicine

Email: biolaber@inbox.ru
ORCID iD: 0000-0002-9925-2886
SPIN-code: 8088-4446
Scopus Author ID: 55822129200

Researcher Associate, Department of General Morphology

Russian Federation, Saint Petersburg

Svetlana V. Maltseva

Institute of Experimental Medicine

Email: pigarevsky@mail.ru
SPIN-code: 8367-9096

PhD (Biology), Researcher Associate, Department of General Morphology

Russian Federation, Saint Petersburg

Natalya G. Davydova

Institute of Experimental Medicine

Email: pigarevsky@mail.ru
SPIN-code: 4761-3575

PhD (Medicine), Researcher Associate, Department of General Morphology

Russian Federation, Saint Petersburg

References

  1. Симбирцев А.С. Цитокины в патогенезе и лечении заболеваний человека. – СПб.: Фолиант, 2018. – 510 с. [Simbirtsev AS. Tsitokiny v patogeneze i lechenii zabolevaniy cheloveka. Saint Petersburg: Foliant; 2018. 510 р. (In Russ.)]
  2. Xie JJ, Wang J, Tang TT, et al. The Th17/Treg functional imbalance during atherogenesis in ApoE(-/-) mice. Cytokine. 2010;49(2):185-193. https://doi.org/10.1016/j.cyto. 2009.09.007.
  3. Ma T, Gao Q, Zhu F, et al. Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice. Cell Mol Immunol. 2013;10(4):338-348. https://doi.org/10.1038/cmi.2013.4.
  4. Tang X. Analysis of interleukin-17 and interleukin-18 levels in animal models of atherosclerosis. Exp Ther Med. 2019;18(1):517-522. https://doi.org/10.3892/etm.2019.7634.
  5. Taleb S, Tedgui A, Mallat Z. Interleukin-17: friend or foe in atherosclerosis? Curr Opin Lipidol. 2010;21(5):404-408. https://doi.org/10.1097/MOL.0b013e32833dc7f9.
  6. Gao Q, Jiang Y, Ma T, et al. A critical function of Th17 proinflammatory cells in the development of atherosclerotic plaque in mice. J Immunol. 2010;185(10):5820-5827. https://doi.org/10.4049/jimmunol.1000116.
  7. Madhur MS, Funt SA, Li L, et al. Role of interleukin 17 in inflammation, atherosclerosis, and vascular function in apolipoprotein e-deficient mice. Arterioscler Thromb Vasc Biol. 2011;31(7):1565-1572. https://doi.org/10.1161/ATVBAHA. 111.227629.
  8. Erbel C, Chen L, Bea F, et al. Inhibition of IL-17A attenuates atherosclerotic lesion development in apoE-deficient mice. J Immunol. 2009;183(12):8167-8175. https://doi.org/10.4049/jimmunol.0901126.
  9. Fatkhullina AR, Peshkova IO, Koltsova EK. The role of cytokines in the development of atherosclerosis. Biokhimiia. 2016;81(11):1358-1370. https://doi.org/10.1134/S0006297916110134.
  10. Пигаревский П.В. Атеросклероз. Нестабильная атеросклеротическая бляшка (иммуноморфологическое исследование): атлас. – СПб.: СпецЛит, 2018. – 148 с. [Pigarevskiy PV. Ateroskleroz. Nestabil’naya ateroskleroticheskaya blyashka (immunomorfologicheskoe issledovanie): atlas. Saint Petersburg: SpetsLit; 2018. 148 p. (In Russ.)]

Supplementary files

Supplementary Files
Action
1. JATS XML
Download
2. Fig. 1. Expression of IL-17 in atherosclerotic damages of an aorta of human. Immunohistochemical staining with use of monoclonal antibodies to IL-17: а — adhesion of the mononuclear cells expressing IL-17 (arrow) on an endothelium of an intima of an unstable plaque in a coronary artery; b — IL-17 expression in cytoplasm of the endothelial cells (arrows) covering a young lipide-fibrous plaque in an aorta; c — the mononuclear cells expressing IL-17 (arrows) around a rupture of a cap of an unstable atherosclerotic plaque; d — lack of IL-17 in an intima of a stable atherosclerotic plaque. а, b — ×630, c, d — ×350

Download (676KB)
Indexing metadata
3. Fig. 2. The quantitative maintenance of endothelial and mononuclear cells expressing IL-17 in normal also in various types of atherosclerotic lesions of an intima of arteries. On an axis of ordinates the quantitative maintenance of cells with IL-17 in 10 fields of microscope is designated

Download (108KB)
Indexing metadata

Copyright (c) 2020 Pigarevsky P.V., Snegova V.A., Maltseva S.V., Davydova N.G.

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: серия ПИ № ФС 77 - 74760 от 29.12.2018 г.