The role of cytomegalovirus and interleukin-8 in destabilization of atherosclerotic lesions in humans

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Abstract

Relevance. Currently, the role of persistent infections in the atherogenesis development mechanism is not fully understood. Therefore, it’s important to analyze the role of viral infection against the background of the pro-inflammatory cytokines expression in atherosclerotic plaque destabilization.

The aim of the work was a comparative immunohistochemical study of cytomegalovirus (CMV) and IL-8 in different types of human atherosclerotic lesions during their destabilization.

Materials and methods. The study was carried out on 130 autopsy samples of human aorta. CMV was detected by direct immunofluorescent antibody staining. IL-8 was detected by two-stage streptavidin-biotin antibody staining.

Results. It has been shown that active detection of both CMV and IL-8 is characteristic of atherogenesis foci of the arterial intima with the most intense immune-inflammatory changes. The obtained results indicate the synergism of the cellular response to CMV and IL-8 in the vascular wall during the destabilization atherosclerotic lesions process.

Conclusion. According to the results of the work, it can be concluded that both the presence of CMV in atherosclerotic lesions and the high production of IL-8 play a significant role in the formation of unstable atherosclerotic plaques in the vascular wall.

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About the authors

Svetlana V. Maltseva

Institute of Experimental Medicine

Author for correspondence.
Email: moon25@rambler.ru
SPIN-code: 8367-9096
Scopus Author ID: 6602920398

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

Russian Federation, Saint Petersburg

Peter V. Pigarevsky

Institute of Experimental Medicine

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

MD, PhD, DSc (Biology), Head of the Department of General Morphology

Russian Federation, Saint Petersburg

Natalya G. Davydova

Institute of Experimental Medicine

Email: tatashaspb@yandex.ru
SPIN-code: 4761-3575

MD, PhD (Medicine), Researcher Associate, 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

Researcher Associate, Department of General Morphology

Russian Federation, Saint Petersburg

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2. Fig. 1. CMV in atherosclerotic aortic lesions. Immunofluorescent staining using FITC, antibodies to cytomegalovirus (a–f: ×1000): a — CMV in the cytoplasm of the endothelial cell in the lipid stain; b — adhesion of the macrophage with CMV in its cytoplasm to the damaged surface of the intima of unstable atherosclerotic plaque; c — CMV in macrophages and SMC in the damaged cap of unstable atherosclerotic plaque; d — CMV in the deep of intima under the connective-tissue cap of unstable atherosclerotic plaque; e — absence CMV in the intimate stable atherosclerotic plaque; f — no CMV in the intima of the normal aortic area

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3. Fig. 2. Cellular inflammatory reactions in the atherogenesis foci: a — numerous endothelial and mononuclear cells expressing IL-8 in the surface departments of the intima of unstable atherosclerotic plaque. Immunohistochemically staining using monoclonal antibodies to IL-8, (×750); b — mononuclear cell infiltration in the surface department of unstable atherosclerotic plaque. Hematoxylin-eosin staining, serial section (×450)

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Copyright (c) 2021 Maltseva S.V., Pigarevsky P.V., Davydova N.G., Snegova V.A.

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
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