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Bee venom phospholipase A2 suppression of experimental autoimmune encephalomyelitis is dependent on its enzymatic activity

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Abstract

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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Acknowledgements

This work was supported by the Basic Science Research Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and Future Planning (NRF-2017R1A2B3009 574).

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Correspondence to Hyunsu Bae.

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Gihyun Lee, Geun-Hyung Kang & Hyunsu Bae declares that they have no conflict of interest.

Human and animal rights

All studies with animals were performed in accordance with the approved animal protocol and guidelines established by the Animal Care and Use Committee of Kyung Hee University. The article does not contain any studies with human.

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Lee, G., Kang, GH. & Bae, H. Bee venom phospholipase A2 suppression of experimental autoimmune encephalomyelitis is dependent on its enzymatic activity. Mol. Cell. Toxicol. 15, 307–313 (2019). https://doi.org/10.1007/s13273-019-0034-8

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  • DOI: https://doi.org/10.1007/s13273-019-0034-8

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