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Review
. 2014 Jun;49(3):1422-34.
doi: 10.1007/s12035-013-8620-6. Epub 2014 Jan 7.

Phagocytosis of microglia in the central nervous system diseases

Ruying Fu  1 , Qingyu Shen, Pengfei Xu, Jin Jun Luo, Yamei Tang
Affiliations
Review

Phagocytosis of microglia in the central nervous system diseases

Ruying Fu et al. Mol Neurobiol. 2014 Jun.

Abstract

Microglia, the resident macrophages of the central nervous system, rapidly activate in nearly all kinds of neurological diseases. These activated microglia become highly motile, secreting inflammatory cytokines, migrating to the lesion area, and phagocytosing cell debris or damaged neurons. During the past decades, the secretory property and chemotaxis of microglia have been well-studied, while relatively less attention has been paid to microglial phagocytosis. So far there is no obvious concordance with whether it is beneficial or detrimental in tissue repair. This review focuses on phagocytic phenotype of microglia in neurological diseases such as Alzheimer's disease, multiple sclerosis, Parkinson's disease, traumatic brain injury, ischemic and other brain diseases. Microglial morphological characteristics, involved receptors and signaling pathways, distribution variation along with time and space changes, and environmental factors that affecting phagocytic function in each disease are reviewed. Moreover, a comparison of contributions between macrophages from peripheral circulation and the resident microglia to these pathogenic processes will also be discussed.

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Conflict of interest statement

The authors declare that there are no conflicts of interest.

Figures

Fig. 1
Fig. 1
Signaling pathways involved in microglial phagocytosis. A Extracellular nucleotides, such as UDP and UTP, trigger microglial phagocytosis through P2Y6R/PLC/InsP3 pathway. B Apoptotic debris induces phagocytosis via TREM-2/DAP12/ERK/PKC pathway. C Endogenous or ectogenic detriments, such as LPS, viral nucleotides, α-synuclein, and f-Aβ, provoke phagocytosis by microglia via TLRs through activation of MyD88-dependent IRAK4/p38/scavenger receptors pathway or MyD88-independent actin-Cdc42/Rac signaling pathway
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