Abstract
In response to environmental stimuli, immune memory mediates the plasticity of myeloid cells. Immune training and immune tolerance are two aspects of plasticity. Microglia that are immunologically trained or immunologically tolerant are endowed with a tendency to differentiate into alternative dominant phenotypes (M1/M2). Male C57BL/6 mice (immune-training group, immune-tolerant group, and control group) were used to establish the kainic acid epilepsy model. The seizure grade, duration, latency, hippocampal potential, and energy density were used to evaluate seizures, and the changes in the polarization of microglia were detected by western blot. 16S rDNA sequencing showed that the abundance of Ruminococcus in the immune-tolerant group was the dominant flora. Our research connections Intestinal microorganisms, brain immune status, and epilepsy behavior together. Pro-inflammatory M1 phenotype and anti-inflammatory M2 phenotype mediate and enhance and suppress subsequent inflammation, respectively. We conclude that intestinal microorganisms influence the occurrence and development of epilepsy by regulating the polarization of microglia.
Highlights
Epilepsy is a chronic disease caused by excessive excitability of brain neurons and sudden abnormal repeated episodes of epileptic discharges, which lead to temporary disorders related to brain function
Compared with the control group, the incubation period of kainic acid (KA)-induced epilepsy was significantly shortened in the immunotraining group, and the seizure incubation period was significantly prolonged in the immunotolerant group (P < 0.01, P < 0.01, Figure 2A)
We investigated whether intestinal microflora can regulate microglial phenotype activation and affect epileptic seizures after inducing immune state change
Summary
Epilepsy is a chronic disease caused by excessive excitability of brain neurons and sudden abnormal repeated episodes of epileptic discharges, which lead to temporary disorders related to brain function. Microglia are immune memory cells in the brain, and their phenotypic changes are important for disease progression. Inhibiting overactivated microglia via inducing phenotype switch from the inflammatory M1 to the protective M2 may be a new therapeutic strategy to alleviate epilepsy (Li et al, 2017; Liu et al, 2018; Deng et al, 2020; Liu et al, 2020). M2 microglia generally play a role in the final stage of an epileptic episode. If the M2 phenotype is activated in the early stage of episode to LPS-Induced Immune Tolerance Improves Epilepsy reduce neuroinflammation, it may be provided beneficial effects to the episode progress. Controlling the M1/M2 polarization ratio of microglia may affect the progression or regression of neuroinflammation in the central nervous system
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