Corrigendum: Phagocytosis in the Brain: Homeostasis and Disease

Galloway, Dylan A.; Phillips, Alexandra; Owen, David R.; Moore, Craig S.

doi:10.3389/fimmu.2019.01575

Cited by 12 publications

(10 citation statements)

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“…The functional plasticity of microglial cells that allows them to carry out a broad repertoire of activities has been reviewed by Gomez-Nicola and Perry (41). Microglia perform continuous surveillance on neurons (34, 35, 42, 43). The pruning of synapses by microglia is an essential part of normal brain development (44).…”

Section: Neuron-microglial Interactions In the Healthy Brainmentioning

confidence: 99%

“…There are billions of neurons in the brain, and a comparable number of microglial cells (61, 62). Microglia perform continuous surveillance on neurons (34, 35, 42, 43). Using in vivo two-photon imaging of the neocortex, Nimmerjahn et al (43), observed that “microglial cells are highly active in their presumed resting state, continually surveying their microenvironment with extremely motile processes and protrusions.” Kierdorf, describing both Nimmerjahn (43) and another two photon imaging study by Davalos et al (63), states that, “two-photon microscopy imaging revealed a strict territorial organization of microglia in vivo … the processes of each microglial cell are highly dynamic, and retract and extend to sample the surrounding CNS.…”

Section: Neuron-microglial Interactions In the Healthy Brainmentioning

confidence: 99%

“…In each of these surveillance events, a microglial cell senses a neuron via multiple signals. The microglial cell will either phagocytize or be inhibited from phagocytizing the neuron, based on the balance of these activating and inhibiting signals (32–34, 63–65). As Brown and Neher have described, microglial cells can incorrectly phagocytize “stressed but viable neurons,” an event they have termed “phagoptosis,” citing evidence that suggests phagoptosis can contribute to neuronal loss during brain development, inflammation, ischemia and neurodegeneration.…”

Section: Neuron-microglial Interactions In the Healthy Brainmentioning

confidence: 99%

“…Both traumatic and non-traumatic insults to brain can trigger mechanisms of ongoing neuronal destruction that are inherently immunological, as microglial cells phagocytize live but marginally functioning neurons (31). Details of the signaling mechanisms that instigate this process have been described by Fricker et al (32) and by Neher et al (33), cited in Galloway et al (34).…”

Section: Introductionmentioning

confidence: 99%

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Microglial Phagocytosis of Neurons: Diminishing Neuronal Loss in Traumatic, Infectious, Inflammatory, and Autoimmune CNS Disorders

Yanuck

2019

Front. Psychiatry

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Errors in neuron-microglial interaction are known to lead to microglial phagocytosis of live neurons and excessive neuronal loss, potentially yielding poorer clinical outcomes. Factors that affect neuron-microglial interaction have the potential to influence the error rate. Clinical comorbidities that unfavorably impact neuron-microglial interaction may promote a higher rate of neuronal loss, to the detriment of patient outcome. This paper proposes that many common, clinically modifiable comorbidities have a common thread, in that they all influence neuron-microglial interactions. Comorbidities like traumatic brain injury, infection, stress, neuroinflammation, loss of neuronal metabolic integrity, poor growth factor status, and other factors, all have the potential to alter communication between neurons and microglia. When this occurs, microglial phagocytosis of live neurons can increase. In addition, microglia can shift into a morphological form in which they express major histocompatibility complex II (MHC-II), allowing them to function as antigen presenting cells that present neuronal debris as antigen to invading T cells. This can increase risk for the development of CNS autoimmunity, or can exacerbate existing CNS autoimmunity. The detrimental influence of these comorbidities has the potential to contribute to the mosaic of factors that determine patient outcome in some CNS pathologies that have neuropsychiatric involvement, including TBI and CNS disorders with autoimmune components, where excessive neuronal loss can yield poorer clinical outcomes. Recognition of the impact of these comorbidities may contribute to an understanding of the common clinical observation that many seemingly disparate factors contribute to the overall picture of case management and clinical outcome in these complex disorders. In a clinical setting, knowing how these comorbidities can influence neuron-microglial interaction can help focus surveillance and care on a broader group of potential therapeutic targets. Accordingly, an interest in the mechanisms underlying the influence of these factors on neuron-microglial interactions is appropriate. Neuron-microglial interaction is reviewed, and the various mechanisms by which these potential comorbidities influence neuro-microglial interaction are described.

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Section: Neuron-microglial Interactions In the Healthy Brainmentioning

confidence: 99%

Section: Neuron-microglial Interactions In the Healthy Brainmentioning

confidence: 99%

Section: Neuron-microglial Interactions In the Healthy Brainmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Microglial Phagocytosis of Neurons: Diminishing Neuronal Loss in Traumatic, Infectious, Inflammatory, and Autoimmune CNS Disorders

Yanuck

2019

Front. Psychiatry

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“…This function is also executed through the production of trophic and synaptogenic factors (Parkhurst et al, 2013;Ueno et al, 2013). In pathological conditions, phagocytic microglia clear cellular debris and pathogens, making way for reparative processes (Galloway et al, 2019b).…”

Section: Microglia In Health and Diseasementioning

confidence: 99%

Dynamic Responses of Microglia in Animal Models of Multiple Sclerosis

Plastini

Desu

Brambilla

2020

Front. Cell. Neurosci.

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Microglia play an essential role in maintaining central nervous system (CNS) homeostasis, as well as responding to injury and disease. Most neurological disorders feature microglial activation, a process whereby microglia undergo profound morphological and transcriptional changes aimed at containing CNS damage and promoting repair, but often resulting in overt inflammation that sustains and propagates the neurodegenerative process. This is especially evident in multiple sclerosis (MS), were microglial activation and microglia-driven neuroinflammation are considered key events in the onset, progression, and resolution of the disease. Our understanding of microglial functions in MS has widened exponentially in the last decade by way of new tools and

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IL-4 and IL-10 promotes phagocytic activity of microglia by up-regulation of TREM2

Jiang²,

Tang

et al. 2020

Cytotechnology

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Corrigendum: Phagocytosis in the Brain: Homeostasis and Disease

Cited by 12 publications

References 0 publications

Microglial Phagocytosis of Neurons: Diminishing Neuronal Loss in Traumatic, Infectious, Inflammatory, and Autoimmune CNS Disorders

Microglial Phagocytosis of Neurons: Diminishing Neuronal Loss in Traumatic, Infectious, Inflammatory, and Autoimmune CNS Disorders

Dynamic Responses of Microglia in Animal Models of Multiple Sclerosis

IL-4 and IL-10 promotes phagocytic activity of microglia by up-regulation of TREM2

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