An enriched environment restores hepatitis B vaccination-mediated impairments in synaptic function through IFN-γ/Arginase1 signaling.

摘要: Activation of the neonatal immune system may contribute to deficits in neuronal plasticity. We have reported that vaccination with a hepatitis B vaccine (HBV) transiently impairs mood status and spatial memory involving systemic T helper (Th) 2 bias M1 microglial activation. Here, an EE induced anti-inflammatory M2 polarization, as evidenced by selectively enhanced expression Arginase1 gene (Arg-1) hippocampus. Interestingly, knock-down Arg-1 prevented effects on restoring dendritic spine density. Moreover, levels Th1-derived cytokine IFN-gamma (IFN-γ) were elevated choroid plexus (CP), which is interface between brain periphery. IFN-γ-blocking antibodies blunted protective density LTP. Furthermore, complement proteins C1q C3 elevated, this elevation was associated synapse loss HBV, whereas reversed HBV. Similarly, blockade activation clearly synaptic pruning microglia, LTP inhibition B-vaccinated mice. Together, EE-induced increase IFN-γ CP disrupt immunosuppression related HBV via IFN-γ/Arg-1/complement-dependent pathway.