Neuroinflammation as secondary damage in head injury
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 ot...
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| Format: | Article |
| Language: | English |
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Research Center of Neurology
2023-03-01
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| Series: | Анналы клинической и экспериментальной неврологии |
| Subjects: | |
| Online Access: | https://annaly-nevrologii.com/journal/pathID/article/viewFile/850/pdf |
| _version_ | 1797849353898950656 |
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| author | Anna E. Karchevskaya Olga V. Payushina Elena V. Sharova Lyubov B. Oknina Oleg Yu. Titov |
| author_facet | Anna E. Karchevskaya Olga V. Payushina Elena V. Sharova Lyubov B. Oknina Oleg Yu. Titov |
| author_sort | Anna E. Karchevskaya |
| collection | DOAJ |
| description | 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-, interleukins (IL)-6 and IL-1, 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. |
| first_indexed | 2024-04-09T18:42:36Z |
| format | Article |
| id | doaj.art-277d1db5940441e9a6c54fe62e04afaa |
| institution | Directory Open Access Journal |
| issn | 2075-5473 2409-2533 |
| language | English |
| last_indexed | 2024-04-09T18:42:36Z |
| publishDate | 2023-03-01 |
| publisher | Research Center of Neurology |
| record_format | Article |
| series | Анналы клинической и экспериментальной неврологии |
| spelling | doaj.art-277d1db5940441e9a6c54fe62e04afaa2023-04-10T17:51:26ZengResearch Center of NeurologyАнналы клинической и экспериментальной неврологии2075-54732409-25332023-03-01171556810.54101/ACEN.2023.1.7635Neuroinflammation as secondary damage in head injuryAnna E. Karchevskaya0https://orcid.org/0000-0001-6647-0572Olga V. Payushina1https://orcid.org/0000-0001-8467-0623Elena V. Sharova2https://orcid.org/0000-0003-4994-4187Lyubov B. Oknina3https://orcid.org/0000-0002-7398-1183Oleg Yu. Titov4https://orcid.org/0000-0001-6570-7777Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of SciencesI.M. Sechenov First Moscow State Medical University (Sechenov University)Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of SciencesInstitute of Higher Nervous Activity and Neurophysiology, Russian Academy of SciencesN.N. Burdenko National Medical Research Center of NeurosurgeryHead 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-, interleukins (IL)-6 and IL-1, 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.https://annaly-nevrologii.com/journal/pathID/article/viewFile/850/pdfneuroinflammationhead injurycytokinestumor necrosis factor-αinterleukinsecondary damagemicroglia |
| spellingShingle | Anna E. Karchevskaya Olga V. Payushina Elena V. Sharova Lyubov B. Oknina Oleg Yu. Titov Neuroinflammation as secondary damage in head injury Анналы клинической и экспериментальной неврологии neuroinflammation head injury cytokines tumor necrosis factor-α interleukin secondary damage microglia |
| title | Neuroinflammation as secondary damage in head injury |
| title_full | Neuroinflammation as secondary damage in head injury |
| title_fullStr | Neuroinflammation as secondary damage in head injury |
| title_full_unstemmed | Neuroinflammation as secondary damage in head injury |
| title_short | Neuroinflammation as secondary damage in head injury |
| title_sort | neuroinflammation as secondary damage in head injury |
| topic | neuroinflammation head injury cytokines tumor necrosis factor-α interleukin secondary damage microglia |
| url | https://annaly-nevrologii.com/journal/pathID/article/viewFile/850/pdf |
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