Abstract
BackgroundAlzheimer’s disease (AD) is a severe neuroinflammatory disease. CD4+Foxp3+ regulatory T cells (Tregs) modulate various inflammatory diseases via suppressing Th cell activation. There are increasing evidences that Tregs have beneficial roles in neurodegenerative diseases. Previously, we found the population of Treg cells was significantly increased by bee venom phospholipase A2 (bvPLA2) treatment in vivo and in vitro.MethodsTo examine the effects of bvPLA2 on AD, bvPLA2 was administered to 3xTg-AD mice, mouse model of Alzheimer’s disease. The levels of amyloid beta (Aβ) deposits in the hippocampus, glucose metabolism in the brain, microglia activation, and CD4+ T cell infiltration were analyzed to evaluate the neuroprotective effect of bvPLA2.ResultsbvPLA2 treatment significantly enhanced the cognitive function of the 3xTg-AD mice and increased glucose metabolism, as assessed with 18F-2 fluoro-2-deoxy-D-glucose ([F-18] FDG) positron emission tomography (PET). The levels of Aβ deposits in the hippocampus were dramatically decreased by bvPLA2 treatment. This neuroprotective effect of bvPLA2 was associated with microglial deactivation and reduction in CD4+ T cell infiltration. Interestingly, the neuroprotective effects of bvPLA2 were abolished in Treg-depleted mice.ConclusionsThe present studies strongly suggest that the increase of Treg population by bvPLA2 treatment might inhibit progression of AD in the 3xTg AD mice.
Highlights
Alzheimer’s disease (AD) is a severe neuroinflammatory disease
Effect of bee venom phospholipase A2 (bvPLA2) treatment on the body weights of the mice The body weights of the wild type (WT), donepeziltreated, bvPLA2-treated, and vehicle-treated 3xTg AD mice were measured every week during the 3-month treatment (Fig. 1a)
The results demonstrated that there were no significant differences in the latency between bvPLA2 and phosphate-buffered saline (PBS) group after regulatory T cells (Tregs) depletion by PC61 anti-CD25 mAb injections (Fig. 5)
Summary
Alzheimer’s disease (AD) is a severe neuroinflammatory disease. CD4+Foxp3+ regulatory T cells (Tregs) modulate various inflammatory diseases via suppressing Th cell activation. There are increasing evidences that Tregs have beneficial roles in neurodegenerative diseases. We found the population of Treg cells was significantly increased by bee venom phospholipase A2 (bvPLA2) treatment in vivo and in vitro. Alzheimer’s disease (AD) is a degenerative disease of the central nervous system. AD is pathologically characterized by extracellular senile plaques, intracellular neurofibrillary tangles, and a reduction of neurons in the cerebral cortex and hippocampus. The clinical features of AD are loss of memory and cognitive and behavioral disorders [1]. AD is one of the most common types of dementia, but its etiology and pathogenesis remain unclear. Various pathological processes are known to be involved in AD.
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