Neuro-protective effects of bee venom by suppression of neuroinflammatory responses in a mouse model of Parkinson’s disease: Role of regulatory T cells

In the present study, we sought to determine whether bee venom (BV) promotes the survival of dopaminergic (DA) neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease (PD). Treatment with BV prevented degeneration of DA neurons in the substantia nigra (SN). This neuro-protective effect of BV was associated with microglial deactivation and reduction of CD4 T cell infiltration. Additionally, BV treatment significantly increased the proportion of CD4+CD25+Foxp3+ Tregs in vivo and in vitro. The increased proportion of Tregs by BV treatment remained suppressive ex vivo. Interestingly, BV treatment did not prevent MPTP neurotoxicity in mice depleted of Tregs by anti-CD25 antibody injection. Therefore, our present studies suggest that modulation of peripheral immune tolerance by Treg may contribute to the neuroprotective effect of BV in the MPTP model of Parkinson’s disease.

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► This work shows that the neuro-protective effect of BV is associated with its antiinflammatory properties in the brain and modulation of peripheral immune tolerance by Tregs.