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KMID : 1034820190150030307
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Molecular & Cellular Toxicology
2019 Volume.15 No. 3 p.307 ~ p.313
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Bee venom phospholipase A2 suppression of experimental autoimmune encephalomyelitis is dependent on its enzymatic activity
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Lee Gi-Hyun
Kang Geun-Hyung
Bae Hyun-Su
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Abstract
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Backgrounds: Bee venom has been used as an alternative medicine for immune-related diseases such as multiple sclerosis (MS). Previously, we showed that Bee venom exerts a therapeutic effect in a mouse model of MS through regulatory T cells (Tregs) and Phospholipase A2 from bee venom (bvPLA2) induces a differentiation of Tregs.
Methods: To induce EAE, C57BL/6 mice were injected MOG35-55 peptide in CFA and pertussis toxin. To ascertain whether Tregs were involved in the neural protective effect of bvPLA2, the mice received a PC61 an-ti-CD25 mAb to deplete Tregs or normal anti-rat IgG1 for an isotype control. To verify the necessity of enzymatic activity experimentally, we synthesized a recombinant bvPLA2 and mutant bvPLA2, which has no catalytic ability.
Results: The limb paralysis caused by EAE was significantly attenuated in the bvPLA2-treated mice compared to the PBS-treated mice. The beneficial effects of bvPLA2 disappeared when Tregs were depleted. Synthetic bvPLA2 showed therapeutic effects such as those of the natural bvPLA2; however, the mutant which has no catalytic ability did not.
Conclusion: Our findings suggest that bvPLA2 contributes to the control of MS and that its catalytic ability is needed for its therapeutic action.
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KEYWORD
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Phospholipase A2, Bee venom, Multiple sclerosis, Experimental autoimmune encephalomyelitis, Enzyme activity
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