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Role of Macrophages and Microglia in the Injured CNS
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
A microglial cell is a resident cell of the CNS. This means that it is distributed ubiquitously throughout the parenchyma and that it is in contact with other macroglial cells and neurons. Resident microglia in the normal CNS are also called ramified, or resting microglia, and these cells are normally not phagocytic (they are resting from phagocytosis). They transform into phagocytes only if degeneration occurs and debris needs to be cleared. Because microglia are present everywhere in the CNS and are the first to encounter any degenerative changes in the parenchyma, they constitute the primary source of brain macrophages. Microglia have the potential to renew their cell pool via mitosis; once they have become activated and transform into microglia-derived brain macrophages their ultimate fate is one of programmed cell death.3
The Promise for Alzheimer’s Disease Treatment
Published in Dilip Ghosh, Pulok K. Mukherjee, Natural Medicines, 2019
Víctor Andrade, Leonardo Guzmán-Martínez, Nicole Cortés, Ricardo B. Maccioni
As mentioned, microglial cells mediate the immune response in the CNS. To accomplish this task, the microglia turn into a functional polarised state, being able to carry out a specific effector program. This brain cellular type exhibits two polarised forms, one of which develops the classical pro-inflammatory response and this is the most common phenotype. The alternative form generates an anti-inflammatory effect directed to heal a zone affected by an acute injury (Jha et al. 2016).
Neuroimmune Mechanisms In The Pathogenesis Of Alzheimer’s Disease
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
Patrick L. McGeer, Edith G. McGeer
The pivotal cell in local immune reactions is the tissue macrophage which, in the case of brain, is the microglial cell. Microglial cells can be activated by a myriad of processes. The precise signaling agents have yet to be identified. Presumably inflammatory cytokines are prominently involved. Upon activation, the microglial cell changes its morphology, with its cytoplasm enlarging, and its ramified processes retracting and thickening. It begins to express high levels of a variety of surface receptors which have as their ligands immune system proteins. Table 1 lists some of these receptor-ligand inflammatory pairs. Many more will undoubtedly be discovered in the future. They illustrate the commonality of genotype between microglial cells and monocytes, in addition to the types of surface reactions these cells undergo.
Novel nano-carriers with N-formylmethionyl-leucyl-phenylalanine-modified liposomes improve effects of C16-angiopoietin 1 in acute animal model of multiple sclerosis
Published in Drug Delivery, 2023
Xiao-Xiao Fu, Han Qu, Jing Wang, Hua-Ying Cai, Hong Jiang, Hao-Hao Chen, Shu Han
In acute EAE models (vehicle group), the CNS demonstrated high leukocyte infiltration that occurred rapidly throughout the brain and spinal cord. At the same time, activated microglia produced a proinflammatory milieu, stripped off myelin from neuronal axons, and attracted activated T-lymphocytes that augmented the destruction of myelin. This study demonstrated that the C + A compounds significantly suppressed the widespread leukocyte infiltration in perivascular and parenchymal areas and reduced the activation of microglia induced by EAE. Activated microglial cells include two phenotypes: neurotoxic M1-like (labeled by CD86) and neuroprotective M2-like (labeled by CD206) cells. M1-like microglia can establish a microenvironment that is detrimental to neurons by producing inflammatory ROS, while M2-like microglia can establish a beneficial microenvironment for neurons by secreting neurotrophic factors and anti-inflammatory mediators (Fu et al., 2020). The results of this study indicated that the C + A compounds could activate the M2 phenotype and suppress the M1 phenotype of microglial cells.
Formononetin Inhibits Microglial Inflammatory Response and Contributes to Spinal Cord Injury Repair by Targeting the EGFR/MAPK Pathway
Published in Immunological Investigations, 2023
Haiping Fu, Mingdong Li, Yanqiang Huan, Xiaolei Wang, Mingkai Tao, Tianqi Jiang, Hongbin Xie, Yongxiong He
Microglial cells are the brain’s immune cells in the central nervous system (CNS). Being derived from myeloid progenitors, microglia play an important role in phagocytes, recognizing, and scavenging dead cells and pathogens (Zhang et al. 2018). Microglia reside in the spinal cord and participate in the progression and neuroinflammation after SCI (Lin et al. 2017). They are activated and secret plenty of pro-inflammatory cytokines and chemokines to aggravate microglial inflammation (Gao et al. 2021). A growing number of studies have demonstrated that microglia activation is one of the main reasons for secondary injury after SCI, and the inhibition of microglia activation reduces spinal cord tissue damage (Finegold 1975; Kalz et al. 1990; Tucker et al. 1997). In addition, a previous study has shown that FMN incubation significantly reduced the production of TNF-α, IL-6, and IL-1β in LPS-stimulated BV2 microglia (El-Bakoush and Olajide 2018). These researches suggest a possibility that FMN may inhibit the microglial inflammatory response after SCI.
Neuroinflammation, immune response and α-synuclein pathology: how animal models are helping us to connect dots
Published in Expert Opinion on Drug Discovery, 2023
Tiziano Balzano, Noelia Esteban-García, Javier Blesa
More proof about the role of microglial cells in the initiation of PD is provided by a study showing that deletion of the fractalkine receptor CX3CR1, present in microglia, monocytes, natural killer and dendritic cells, reduces rAAV2-α-syn induced inflammation [51]. All together, these studies suggest that targeting signaling involved in inflammatory pathways promoted by microglial cells may provide therapeutic targets to prevent or slow down PD progression. More evidence suggesting that neuroinflammatory processes are closely linked to dopaminergic cell death is given in [52]. These authors show in a rAAV2/7 α-syn rat model that treatment with the immunophilin ligand FK506, a neuroprotective drug, increased the survival of dopaminergic neurons by reducing infiltration of both T helper and cytotoxic T cells as well as the number and subtype of microglia and macrophages, but not α-syn aggregation. These findings emphasize that neuroinflammatory processes and immune response rather than α-synucleinopathy have a direct, causal role in the pathogenesis of PD [52].