High-Intensity Exercise Training Protects the Brain Against Autoimmune Neuroinflammation: Regulation of Microglial Redox and Pro-inflammatory Functions

Background : Exercise training induces beneficial effects on neurodegenerative diseases, and specifically multiple sclerosis (MS) it’s model experimental autoimmune encephalomyelitis (EAE). However, it is unclear whether exercise exerts direct protective the central nervous system (CNS), nor are mechanisms of neuroprotection fully understood. In this study, we investigated neuroprotective high-intensity continuous (HICT) against development neuroinflammation role resident microglia. Methods We used transfer EAE to examine CNS. Healthy mice performed HICT by treadmill running, followed injection encephalitogenic proteolipid (PLP)-reactive T-cells induce EAE. severity was assessed clinically pathologically. Brain microglia from sedentary (SED) healthy mice, as well 5-days post induction (before onset disease), were analyzed ex vivo for reactive oxygen species (ROS) nitric oxide (NO) formation, mRNA expression M1/M2 markers neurotrophic factors, secretion cytokines chemokines. Results Transfer into resulted in milder EAE, compared indicated reduced clinical severity, attenuated T-cell, neurotoxic macrophage/microglial infiltration, loss myelin axons. number without affecting their profile. Isolated after exhibited ROS formation released less IL-6 monocyte chemoattractant protein (MCP) response PLP-stimulation. Conclusions These findings point critical intensity neuroprotection. protects CNS reducing microglial-derived neurotoxicity, pro-inflammatory responses involved propagation neuroinflammation.