Proinflammatory mediators released by activated microglia induces neuronal death in Japanese encephalitis

Glia ◽  
2007 ◽  
Vol 55 (5) ◽  
pp. 483-496 ◽  
Author(s):  
Ayan Ghoshal ◽  
Sulagna Das ◽  
Soumya Ghosh ◽  
Manoj Kumar Mishra ◽  
Vivek Sharma ◽  
...  
Keyword(s):  
Japanese Encephalitis ◽  
Neuronal Death ◽  
Activated Microglia ◽  
Proinflammatory Mediators

Heterogeneity of Microglia Phenotypes: Developmental, Functional and Some Therapeutic Considerations

2019 ◽  
Vol 25 (21) ◽  
pp. 2375-2393 ◽  
Author(s):  
Yun Yuan ◽  
Chunyun Wu ◽  
Eng-Ang Ling
Keyword(s):  
Brain Lesion ◽  
Translocator Protein ◽  
Trophic Factors ◽  
Microglial Cells ◽  
Brain Maturation ◽  
Activated Microglia ◽  
Proinflammatory Mediators ◽  
Pathological Conditions ◽  
Positron Emission ◽  
M2 Microglia

Background: Microglia play a pivotal role in maintaining homeostasis in complex brain environment. They first exist as amoeboid microglial cells (AMCs) in the developing brain, but with brain maturation, they transform into ramified microglial cells (RMCs). In pathological conditions, microglia are activated and have been classified into M1 and M2 phenotypes. The roles of AMCs, RMCs and M1/M2 microglia phenotypes especially in pathological conditions have been the focus of many recent studies. Methods: Here, we review the early development of the AMCs and RMCs and discuss their specific functions with reference to their anatomic locations, immunochemical coding etc. M1 and M2 microglia phenotypes in different neuropathological conditions are also reviewed. Results: Activated microglia are engaged in phagocytosis, production of proinflammatory mediators, trophic factors and synaptogenesis etc. Prolonged microglia activation, however, can cause damage to neurons and oligodendrocytes. The M1 and M2 phenotypes featured prominently in pathological conditions are discussed in depth. Experimental evidence suggests that microglia phenotype is being modulated by multiple factors including external and internal stimuli, local demands, epigenetic regulation, and herbal compounds. Conclusion: Prevailing views converge that M2 polarization is neuroprotective. Thus, proper therapeutic designs including the use of anti-inflammatory drugs, herbal agents may be beneficial in suppression of microglial activation, especially M1 phenotype, for amelioration of neuroinflammation in different neuropathological conditions. Finally, recent development of radioligands targeting 18 kDa translocator protein (TSPO) in activated microglia may hold great promises clinically for early detection of brain lesion with the positron emission tomography.

scholarly journals Glial activation involvement in neuronal death by Japanese encephalitis virus infection

2009 ◽  
Vol 91 (4) ◽  
pp. 1028-1037 ◽  
Author(s):  
C.-J. Chen ◽  
Y.-C. Ou ◽  
S.-Y. Lin ◽  
S.-L. Raung ◽  
S.-L. Liao ◽  
...  
Keyword(s):  
Virus Infection ◽  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Neuronal Death ◽  
Encephalitis Virus ◽  
Glial Activation ◽  
Japanese Encephalitis Virus Infection

scholarly journals Reciprocal modulation of C/EBP-α and C/EBP-β by IL-13 in activated microglia prevents neuronal death

2013 ◽  
Vol 43 (11) ◽  
pp. 2854-2865 ◽  
Author(s):  
Hung Chuan Pan ◽  
Cheng Ning Yang ◽  
Yi Wen Hung ◽  
Wen Jane Lee ◽  
Hsing Ru Tien ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Activated Microglia

scholarly journals Roles of TLR3 and RIG-I in Mediating the Inflammatory Response in Mouse Microglia following Japanese Encephalitis Virus Infection

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Rong Jiang ◽  
Jing Ye ◽  
Bibo Zhu ◽  
Yunfeng Song ◽  
Huanchun Chen ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Neuronal Damage ◽  
Central Nervous System Disease ◽  
Encephalitis Virus ◽  
Mitogen Activated Protein Kinase ◽  
Japanese Encephalitis Virus Infection ◽  
Proinflammatory Mediators ◽  
System Disease

Japanese encephalitis virus (JEV) infection can cause central nervous system disease with irreversible neurological damage in humans and animals. Evidence suggests that overactivation of microglia leads to greatly increased neuronal damage during JEV infection. However, the mechanism by which JEV induces the activation of microglia remains unclear. Toll-like receptor 3 (TLR3) and retinoic acid-inducible gene I (RIG-I) can recognize double-stranded RNA, and their downstream signaling results in production of proinflammatory mediators. In this study, we investigated the roles of TLR3 and RIG-I in the inflammatory response caused by JEV infection in the mouse microglial cell line. JEV infection induced the expression of TLR3 and RIG-I and the activation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38MAPK). Knockdown of TLR3 and RIG-I attenuated activation of ERK, p38MAPK, activator protein 1 (AP-1), and nuclear factorκB (NF-κB). Secretion of TNF-α, IL-6, and CCL-2, which was induced by JEV, was reduced by TLR3 and RIG-I knockdown and inhibitors of phosphorylated ERK and p38MAPK. Furthermore, viral proliferation was increased following knockdown of TLR3 and RIG-I. Our findings suggest that the signaling pathways of TLR3 and RIG-I play important roles in the JEV-induced inflammatory response of microglia.

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