Neuroinflammation as secondary damage in head injury

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Abstract

Head injury is one of the main disability causes among the working-age population. Stroke energy induces mechanical injury of tissues to launch secondary damage, i.e. neurotransmission, blood-brain barrier disruption, blood infiltration of brain tissues, cytokine and chemokine overexpression, and other processes. Activated by the injury, microglia plays a special part to initially 'protect' intact tissues from the products of necrosis and apoptosis. After the injury, microglia rapidly differentiates to phenotypes М1 and М2. Pro-inflammatory phenotype М1 produces neuronal cytotoxic cytokines including tumor necrosis factor-α, interleukins (IL)-6 and IL-1β, and NO that induce apoptosis while phenotype М2 secretes IL-4 and IL-13 that may supposedly reduce inflammation and improve recovery of brain tissues. М2 response lasts much less than М1 response, and increasing pro-inflammatory activation leads to further neuronal death, which affects cognitive and physical status of patients with head injury. The review covers main biochemical processes in the injured brain and possible ways of neuroinflammation modulation.

About the authors

Anna E. Karchevskaya

Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences; I.M. Sechenov First Moscow State Medical University (Sechenov University); N.N. Burdenko National Medical Research Center of Neurosurgery

Author for correspondence.
Email: ankar1998@yandex.ru
ORCID iD: 0000-0001-6647-0572

Junior Researcher, Laboratory of General and Clinical Neurophysiology, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences; Student, I.M. Sechenov First Moscow State Medical University (Sechenov University); Clinical Psychologist, N.N. Burdenko National Medical Research Center of Neurosurgery

Russian Federation, Moscow; Moscow; Moscow

Olga V. Payushina

I.M. Sechenov First Moscow State Medical University (Sechenov University)

Email: payushina@mail.ru
ORCID iD: 0000-0001-8467-0623

D. Sci. (Biol.), Associate Professor, Department of Histology, Cytology and Embryology, I.M. Sechenov First Moscow State Medical University (Sechenov University)

Russian Federation, Moscow

Elena V. Sharova

Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences

Email: ESharova@nsi.ru
ORCID iD: 0000-0003-4994-4187
SPIN-code: 5233-9615
Scopus Author ID: 7003870497

D. Sci. (Biol.), Head, Laboratory of General and Clinical Neurophysiology, Institute of Higher Nervous Activity and Neurophysiology

Russian Federation, Moscow

Lyubov B. Oknina

Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences

Email: lyubov.oknina@ihna.ru
ORCID iD: 0000-0002-7398-1183
SPIN-code: 2614-8209
Scopus Author ID: 6602961277

D. Sci. (Biol.), Senior Researcher, Laboratory of General and Clinical Neurophysiology, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences

Russian Federation, Moscow

Oleg Yu. Titov

N.N. Burdenko National Medical Research Center of Neurosurgery

Email: neurolegtitov@gmail.com
ORCID iD: 0000-0001-6570-7777

Postgraduate Student, N.N. Burdenko National Medical Research Center of Neurosurgery

Russian Federation, Moscow

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2. Fig. 1. Brain damage and physiological changes associated with head injury.

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3. Fig. 2. Mechanical brain injury causes acute neuronal death, brain tissue damage, and blood-brain barrier (BBB) disruption followed by neutrophil migration to the brain tissues. Then microglia, astroglia, and leukocytes start producing cytokines and chemokines. Microglia differentiates into two subtypes, M1 and M2, and an M1 pro-inflammatory response lasts longer than an anti-inflammatory one. Astrocytes induce glial scarification. Elevated cytokine levels, accumulation of neural collapse products, and neurochemical abnormalities launch pro-apoptotic cascade.

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