Epiplexus phagocytes of nervous tissue in experimental brain contusion

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Abstract

Neuroinflammation is known to participate in pathogenesis of intracranial brain injury (TBI), e.g., brain contusion or concussion. In view of high overall prevalence of these conditions, there is a need for nosological verification of the mild- and moderate-severity neuroinflammation. Our research in immune regulation of blood flow in TBI, including a role of Kolmer cells in pathogenesis of neuroinflammation, is now at the stage of collecting research data and requires adequate experimental study. Purpose of our study was as follows: to assess the state of Kolmer cells in vascular plexus of brain ventricles in experimental model of mild traumatic brain contusion (mTBC). mTBC was reproduced in male Wistar rats using a model of a falling load weighing 200 g. Immunohistochemical study was performed in order to assess CD45 receptor expression on the brain cells. During acute period after mTBC, we observed constriction of blood vessels and pericellular edema of the brain tissues. Expression of CD45 cytodifferentiation receptors markers characteristic of the hematopoietic cell pools was found in parenchymal areas of neocortex and on the surface of choroid plexuses in brain ventricles. These data suggest participation of epiplexus and parenchymal macrophages in the pronounced pericellular edema of the brain. On the 8th day of observation, the spasm of the blood vessels persists, along with significantly weaker pericellular edema. In all the brain sections, leukocyte infiltration of tissues was not seen, and there was no expression of CD45 receptors, whereas increased number and size of nucleoli was found in the neurons. The results of our study confirm the role of cerebral vasospasm as a severe complication of neuroinflammation developing after mTBI. Acute inflammation is characterized by a series of vascular changes, manifesting by development of vasospasm, arterial, venous hyperemia and stasis. Venous hyperemia is characterized by further vasodilation, tissue plethora, the phenomenon of the marginal leukocyte stasis and their emigration, along with increased exudation processes. Innervation from subcortical neurons or local cortical interneurons to parenchymal arterioles and cortical microvessels provides minimal contact and predominantly targets the surrounding astrocytes and other cells. During acute period of mTBC, the inflammatory process is confirmed by the presence in parenchyma and on the surface of ependymal Kolmer cells and by expression of CD45 receptors. This finding points to inflammatory reasons for altered tone of pial blood vessels, capillaries of neocortex and ependymal areas, and changed depth of subarachnoid space. Response of astrocytes to the brain trauma could be another factor of neuroinflammation.

About the authors

N. G. Plekhova

Pacific State Medical University

Author for correspondence.
Email: pl_nat@hotmail.com

Natalia G. Plekhova - PhD, MD (Biology), Head, Central Research Laboratory, Pacific State Medical University.

690002, Vladivostok, Ostryakov ave., 2.

Phone: 7 (914) 672-69-53.

Russian Federation

S. V. Zinoviev

Pacific State Medical University

Email: Sinowev@mail.ru

PhD (Medicine), Senior Researcher, Central Research Laboratory, Pacific State Medical University.

690002, Vladivostok, Ostryakov ave., 2.

Russian Federation

E. V. Prosekova

Pacific State Medical University

Email: kld_oki_tgmu@mail.ru

PhD, MD (Medicine), Professor, Head of Department of Clinical Laboratory Diagnostics, General and Clinical Immunology, Pacific State Medical University.

690002, Vladivostok, Ostryakov ave., 2.

Russian Federation

I. V. Radkov

Pacific State Medical University

Email: radiarest@gmail.com

Junior Researcher, Central Research Laboratory, Pacific State Medical University.

690002, Vladivostok, Ostryakov ave., 2.

Russian Federation

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Copyright (c) 2021 Plekhova N.G., Zinoviev S.V., Prosekova E.V., Radkov I.V.

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This work is licensed under a Creative Commons Attribution 4.0 International License.
Свидетельство о регистрации СМИ ПИ № 77 - 11525 от 04.01.2002 выдано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).


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