Abstract
The interaction between microglia and astrocytes significantly influences neuroinflammation. Microglia/astrocytes, part of the neurovascular unit (NVU), are activated by various brain insults. The local extracellular and intracellular signals determine their characteristics and switch of phenotypes. Microglia and astrocytes are activated into two polarization states: the pro-inflammatory phenotype (M1 and A1) and the anti-inflammatory phenotype (M2 and A2). During neuroinflammation, induced by stroke or lipopolysaccharides, microglia are more sensitive to pathogens, or damage; they are thus initially activated into the M1 phenotype and produce common inflammatory signals such as IL-1 and TNF-α to trigger reactive astrocytes into the A1 phenotype. These inflammatory signals can be amplified not only by the self-feedback loop of microglial activation but also by the unique anatomy structure of astrocytes. As the pathology further progresses, resulting in local environmental changes, M1-like microglia switch to the M2 phenotype, and M2 crosstalk with A2. While astrocytes communicate simultaneously with neurons and blood vessels to maintain the function of neurons and the blood–brain barrier (BBB), their subtle changes may be identified and responded by astrocytes, and possibly transferred to microglia. Although both microglia and astrocytes have different functional characteristics, they can achieve immune “optimization” through their mutual communication and cooperation in the NVU and build a cascaded immune network of amplification.
Highlights
Neuroinflammation often runs through the entire process of pathological development
Neuroinflammation is dynamic with the regulation of pro and anti-inflammatory signals
The activation and interaction of glial cells play a crucial role at different stages of pathology in Central nervous system (CNS) disorders
Summary
Li-rong Liu 1,2†, Jia-chen Liu 3†, Jin-shuang Bao 1, Qin-qin Bai 1 and Gai-qing Wang 1,4*. During neuroinflammation, induced by stroke or lipopolysaccharides, microglia are more sensitive to pathogens, or damage; they are initially activated into the M1 phenotype and produce common inflammatory signals such as IL-1 and TNF-α to trigger reactive astrocytes into the A1 phenotype. These inflammatory signals can be amplified by the self-feedback loop of microglial activation and by the unique anatomy structure of astrocytes. While astrocytes communicate simultaneously with neurons and blood vessels to maintain the function of neurons and the blood–brain barrier (BBB), their subtle changes may be identified and responded by astrocytes, and possibly transferred to microglia. Both microglia and astrocytes have different functional characteristics, they can achieve immune “optimization” through their mutual communication and cooperation in the NVU and build a cascaded immune network of amplification
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have