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Published on: March 9, 2018
Curcumin-dependent phenotypic transformation of microglia mediates resistance to pseudorabies-induced encephalitis
Luqiu Feng1, Guodong Luo1, Yuhang Li1
1College of Veterinary Medicine, Southwest University, Chongqing, 402460, China.
Abstract:
Pseudorabies virus (PRV) causes viral encephalitis, a devastating disease with high mortality worldwide. Curcumin (CUR) can reduce inflammatory damage by altering the phenotype of microglia; however, whether and how these changes mediate resistance to PRV-induced encephalitis is still unclear. In this study, BV2 cells were infected with/without PRV for 24 h and further treated with/without CUR for 24 h. The results indicated that CUR promoted the polarization of PRV-infected BV2 cells from the M1 phenotype to the M2 phenotype and reversed PRV-induced mitochondrial dysfunction. Furthermore, M1 BV2 cell secretions induced signalling pathways leading to apoptosis in PC-12 neuronal cells, and this effect was abrogated by the secretions of M2 BV2 cells. RNA sequencing and bioinformatics analysis predicted that this phenotypic shift may be due to changes in energy metabolism. Furthermore, Western blot analysis showed that CUR inhibited the increase in AMP-activated protein kinase (AMPK) phosphorylation, glycolysis, and triacylglycerol synthesis and the reduction in oxidative phosphorylation induced by PRV infection. Moreover, the ATP levels in M2 BV2 cells were higher than those in M1 cells. Furthermore, CUR prevented the increase in mortality, elevated body temperature, slowed growth, nervous system excitation, brain tissue congestion, vascular cuffing, and other symptoms of PRV-induced encephalitis in vivo. Thus, this study demonstrated that CUR protected against PRV-induced viral encephalitis by switching the phenotype of BV2 cells, thereby protecting neurons from inflammatory injury, and this effect was mediated by improving mitochondrial function and the AMPK/NF-κB p65-energy metabolism-related pathway.
Insights
Curcumin (CUR) protects against pseudorabies virus (PRV)-induced encephalitis by shifting microglia from M1 to M2 phenotypes. This improves mitochondrial function and energy metabolism, ultimately protecting neurons from inflammatory damage.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Pseudorabies virus (PRV) causes severe, high-mortality viral encephalitis.
- Curcumin (CUR) is known to modulate microglial inflammatory responses, but its specific role in PRV encephalitis is not fully understood.
- Understanding microglial phenotype changes is crucial for developing effective treatments against PRV-induced neurological damage.
Purpose of the Study:
- To investigate whether curcumin (CUR) can protect against PRV-induced viral encephalitis.
- To elucidate the mechanisms by which CUR alters microglial phenotypes and impacts neuronal survival.
- To explore the role of energy metabolism and mitochondrial function in CUR's protective effects against PRV.
Main Methods:
- BV2 microglial cells were infected with PRV and treated with CUR.
- Phenotypic polarization (M1/M2), mitochondrial function, and energy metabolism (AMPK, glycolysis, oxidative phosphorylation) were assessed.
- Neuronal apoptosis induced by M1 microglia secretions was evaluated.
- In vivo studies assessed CUR's efficacy in mitigating PRV encephalitis symptoms and mortality.
Main Results:
- CUR promoted PRV-infected BV2 cells to polarize from M1 to M2 phenotype, reversing PRV-induced mitochondrial dysfunction.
- M1 microglia secretions induced neuronal apoptosis, while M2 secretions abrogated this effect.
- CUR inhibited PRV-induced increases in AMPK phosphorylation, glycolysis, and triacylglycerol synthesis, while restoring oxidative phosphorylation.
- CUR treatment reduced PRV-induced mortality, fever, neurological symptoms, and brain pathology in vivo.
Conclusions:
- Curcumin (CUR) confers protection against PRV-induced viral encephalitis.
- CUR achieves this by switching microglia from an M1 to an M2 phenotype, improving mitochondrial function and energy metabolism.
- The protective mechanism involves the AMPK/NF-κB p65-energy metabolism pathway, ultimately safeguarding neurons from inflammatory injury.
