Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury

Mechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradi...

Olles dieđut

Furkejuvvon:
Bibliográfalaš dieđut
Váldodahkkit: Arthur Liesz, Christoph Kleinschnitz
Materiálatiipa: Online
Giella:eaŋgalasgiella
Almmustuhtton: Frontiers Media SA 2021
Fáttát:
Liŋkkat:18820
Fáddágilkorat: Lasit fáddágilkoriid
Eai fáddágilkorat, Lasit vuosttaš fáddágilkora!
_version_ 1869514833436606464
author Arthur Liesz
Christoph Kleinschnitz
author_browse Arthur Liesz
Christoph Kleinschnitz
author_facet Arthur Liesz
Christoph Kleinschnitz
author_sort Arthur Liesz
collection Directory of Open Access Books
description Mechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradigms like ischemic stroke, intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Resident microglial cells sense tissue damage and initiate inflammation, activation of the endothelial brain-immune interface promotes recruitment of systemic immune cells to the brain and systemic humoral immune mediators (e.g. complements and cytokines) enter the brain through the damaged blood-brain barrier. These cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute substantially to secondary brain damage and neurodegeneration. Diverse inflammatory cascades such as pro-inflammatory cytokine secretion of invading leukocytes and direct cell-cell-contact cytotoxicity between lymphocytes and neurons have been demonstrated to mediate the inflammatory ‘collateral damage’ in models of acute brain injury. Besides mediating neuronal cell loss and degeneration, secondary inflammatory mechanisms also contribute to functional modulation of neurons and the impact of post-lesional neuroinflammation can even be detected on the behavioral level. The contribution of several specific immune cell subpopulations to the complex orchestration of secondary neuroinflammation has been revealed just recently. However, the differential vulnerability of specific neuronal cell types and the molecular mechanisms of inflammatory neurodegeneration are still elusive. Furthermore, we are only on the verge of characterizing the control of long-term recovery and neuronal plasticity after brain damage by inflammatory pathways. Yet, a more detailed but also comprehensive understanding of the multifaceted interaction of these two supersystems is of direct translational relevance. Immunotherapeutic strategies currently shift to the center of translational research in acute CNS lesion since all clinical trials investigating direct neuroprotective therapies failed. To advance our knowledge on brain-immune communications after brain damage an interdisciplinary approach covered by cellular neuroscience as well as neuroimmunology, brain imaging and behavioral sciences is crucial to thoroughly depict the intricate mechanisms.
format Online
id doab-20.500.12854ir-52948
institution Directory of Open Access Books
language eng
publishDate 2021
publishDateRange 2021
publishDateSort 2021
publisher Frontiers Media SA
publisherStr Frontiers Media SA
record_format ojs
spelling doab-20.500.12854ir-529482024-04-05T12:35:26Z Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury Arthur Liesz Christoph Kleinschnitz RC321-571 Q1-390 intracerebral hemorrhage Stroke Traumatic Brain Injury Cytokines neurodegeneration Neuroinflammation Leukocytes Immunity thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences Mechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradigms like ischemic stroke, intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Resident microglial cells sense tissue damage and initiate inflammation, activation of the endothelial brain-immune interface promotes recruitment of systemic immune cells to the brain and systemic humoral immune mediators (e.g. complements and cytokines) enter the brain through the damaged blood-brain barrier. These cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute substantially to secondary brain damage and neurodegeneration. Diverse inflammatory cascades such as pro-inflammatory cytokine secretion of invading leukocytes and direct cell-cell-contact cytotoxicity between lymphocytes and neurons have been demonstrated to mediate the inflammatory ‘collateral damage’ in models of acute brain injury. Besides mediating neuronal cell loss and degeneration, secondary inflammatory mechanisms also contribute to functional modulation of neurons and the impact of post-lesional neuroinflammation can even be detected on the behavioral level. The contribution of several specific immune cell subpopulations to the complex orchestration of secondary neuroinflammation has been revealed just recently. However, the differential vulnerability of specific neuronal cell types and the molecular mechanisms of inflammatory neurodegeneration are still elusive. Furthermore, we are only on the verge of characterizing the control of long-term recovery and neuronal plasticity after brain damage by inflammatory pathways. Yet, a more detailed but also comprehensive understanding of the multifaceted interaction of these two supersystems is of direct translational relevance. Immunotherapeutic strategies currently shift to the center of translational research in acute CNS lesion since all clinical trials investigating direct neuroprotective therapies failed. To advance our knowledge on brain-immune communications after brain damage an interdisciplinary approach covered by cellular neuroscience as well as neuroimmunology, brain imaging and behavioral sciences is crucial to thoroughly depict the intricate mechanisms. 2021-02-11T19:01:21Z 2021-02-11T19:01:21Z 2016-04-07 11:22:02 2015 book 18820 16648714 9782889196913 https://directory.doabooks.org/handle/20.500.12854/52948 eng Frontiers Research Topics image/jpeg Attribution 4.0 International http://www.frontiersin.org/books/Mechanisms_of_neuroinflammation_and_inflammatory_neurodegeneration_in_acute_brain_injury/725#nogo http://journal.frontiersin.org/researchtopic/2781/mechanisms-of-neuroinflammation-and-inflammatory-neurodegeneration-in-acute-brain-injury Frontiers Media SA 10.3389/978-2-88919-691-3 10.3389/978-2-88919-691-3 bf5ce210-e72e-4860-ba9b-c305640ff3ae 9782889196913 284 open access
spellingShingle RC321-571
Q1-390
intracerebral hemorrhage
Stroke
Traumatic Brain Injury
Cytokines
neurodegeneration
Neuroinflammation
Leukocytes
Immunity
thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences
Arthur Liesz
Christoph Kleinschnitz
Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
title Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
title_full Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
title_fullStr Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
title_full_unstemmed Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
title_short Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
title_sort mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury
topic RC321-571
Q1-390
intracerebral hemorrhage
Stroke
Traumatic Brain Injury
Cytokines
neurodegeneration
Neuroinflammation
Leukocytes
Immunity
thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences
topic_facet RC321-571
Q1-390
intracerebral hemorrhage
Stroke
Traumatic Brain Injury
Cytokines
neurodegeneration
Neuroinflammation
Leukocytes
Immunity
thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences
url 18820
work_keys_str_mv AT arthurliesz mechanismsofneuroinflammationandinflammatoryneurodegenerationinacutebraininjury
AT christophkleinschnitz mechanismsofneuroinflammationandinflammatoryneurodegenerationinacutebraininjury