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      Cellular infiltration in traumatic brain injury

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          Abstract

          Traumatic brain injury leads to cellular damage which in turn results in the rapid release of damage-associated molecular patterns (DAMPs) that prompt resident cells to release cytokines and chemokines. These in turn rapidly recruit neutrophils, which assist in limiting the spread of injury and removing cellular debris. Microglia continuously survey the CNS (central nervous system) compartment and identify structural abnormalities in neurons contributing to the response. After some days, when neutrophil numbers start to decline, activated microglia and astrocytes assemble at the injury site—segregating injured tissue from healthy tissue and facilitating restorative processes. Monocytes infiltrate the injury site to produce chemokines that recruit astrocytes which successively extend their processes towards monocytes during the recovery phase. In this fashion, monocytes infiltration serves to help repair the injured brain. Neurons and astrocytes also moderate brain inflammation via downregulation of cytotoxic inflammation. Depending on the severity of the brain injury, T and B cells can also be recruited to the brain pathology sites at later time points.

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          Macrophage plasticity and polarization: in vivo veritas.

          Diversity and plasticity are hallmarks of cells of the monocyte-macrophage lineage. In response to IFNs, Toll-like receptor engagement, or IL-4/IL-13 signaling, macrophages undergo M1 (classical) or M2 (alternative) activation, which represent extremes of a continuum in a universe of activation states. Progress has now been made in defining the signaling pathways, transcriptional networks, and epigenetic mechanisms underlying M1-M2 or M2-like polarized activation. Functional skewing of mononuclear phagocytes occurs in vivo under physiological conditions (e.g., ontogenesis and pregnancy) and in pathology (allergic and chronic inflammation, tissue repair, infection, and cancer). However, in selected preclinical and clinical conditions, coexistence of cells in different activation states and unique or mixed phenotypes have been observed, a reflection of dynamic changes and complex tissue-derived signals. The identification of mechanisms and molecules associated with macrophage plasticity and polarized activation provides a basis for macrophage-centered diagnostic and therapeutic strategies.
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            Fate mapping analysis reveals that adult microglia derive from primitive macrophages.

            Microglia are the resident macrophages of the central nervous system and are associated with the pathogenesis of many neurodegenerative and brain inflammatory diseases; however, the origin of adult microglia remains controversial. We show that postnatal hematopoietic progenitors do not significantly contribute to microglia homeostasis in the adult brain. In contrast to many macrophage populations, we show that microglia develop in mice that lack colony stimulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice. In vivo lineage tracing studies established that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8. These results identify microglia as an ontogenically distinct population in the mononuclear phagocyte system and have implications for the use of embryonically derived microglial progenitors for the treatment of various brain disorders.
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              The M1 and M2 paradigm of macrophage activation: time for reassessment

              Macrophages are endowed with a variety of receptors for lineage-determining growth factors, T helper (Th) cell cytokines, and B cell, host, and microbial products. In tissues, macrophages mature and are activated in a dynamic response to combinations of these stimuli to acquire specialized functional phenotypes. As for the lymphocyte system, a dichotomy has been proposed for macrophage activation: classic vs. alternative, also M1 and M2, respectively. In view of recent research about macrophage functions and the increasing number of immune-relevant ligands, a revision of the model is needed. Here, we assess how cytokines and pathogen signals influence their functional phenotypes and the evidence for M1 and M2 functions and revisit a paradigm initially based on the role of a restricted set of selected ligands in the immune response.
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                Author and article information

                Contributors
                alam.camb@gmail.com
                Journal
                J Neuroinflammation
                J Neuroinflammation
                Journal of Neuroinflammation
                BioMed Central (London )
                1742-2094
                3 November 2020
                3 November 2020
                2020
                : 17
                : 328
                Affiliations
                [1 ]GRID grid.5335.0, ISNI 0000000121885934, Division of Neurosurgery, Department of Clinical Neurosciences, , University of Cambridge, ; Cambridge, UK
                [2 ]GRID grid.4714.6, ISNI 0000 0004 1937 0626, Department of Clinical Neuroscience, , Karolinska Institutet, ; Stockholm, Sweden
                [3 ]GRID grid.24381.3c, ISNI 0000 0000 9241 5705, Department of Neurology, , Karolinska University Hospital, ; Stockholm, Sweden
                [4 ]GRID grid.17063.33, ISNI 0000 0001 2157 2938, Injury Prevention Research Office, Division of Neurosurgery, St. Michael’s Hospital, , University of Toronto, ; Toronto, Canada
                [5 ]GRID grid.83440.3b, ISNI 0000000121901201, Department of Neuromuscular Diseases, Queen Square Institute of Neurology, , University College London, ; London, UK
                [6 ]GRID grid.451388.3, ISNI 0000 0004 1795 1830, The Francis Crick Institute, ; London, UK
                Author information
                http://orcid.org/0000-0001-8089-6721
                Article
                2005
                10.1186/s12974-020-02005-x
                7640704
                33143727
                a2ff2d40-59c9-4410-bab8-3d7ecfc8021c
                © The Author(s) 2020

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 10 September 2020
                : 21 October 2020
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100000265, Medical Research Council;
                Award ID: MR/R005036/1
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100010897, Newton Fund;
                Award ID: NF170920
                Award Recipient :
                Categories
                Review
                Custom metadata
                © The Author(s) 2020

                Neurosciences
                neuroinflammation,cellular infiltration,traumatic brain injury,microglial dynamics

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