Bee venom (BV) is one of the most traditional medicines that have been widely used in the treatment of chronic inflammatory diseases, such as rheumatoid arthritis. In the previous study, we reported that BV induced immune tolerance by increasing the population of regulatory T cells (Tregs) in lupus nephritis, cisplatin-induced nephrotoxicity and allergic asthma model. But what component and how it regulates the immune response is mostly unclear. Here, we investigated whether bee venom phospholipase A2 (bvPLA2) has protective effects that are mediated via Tregs in OVA-induced allergic asthma model. We found that bvPLA2 treatment increased the Treg population and suppressed the production of Th2 cytokines in the airways of OVA-induced asthma mice. To assess the involvement of Treg in the bvPLA2 effects, Treg were depleted by anti-CD25 mAb. Although bvPLA2 significantly reduced the number of inflammatory cells in the lung parenchyma and the BAL fluid after OVA challenge, these effects were not observed in Treg-depleted mice. In addition, CD206-deficiency showed the bvPLA2-mediated attenuation of airway inflammation depended on the binding to its receptor, macrophage mannose receptor (CD206). Our results strongly suggest that bvPLA2 has potential as an effective agent on Treg recruitment into the airway for controlling allergic asthma.
Acknowledgement : This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean government (Ministry of Education, Science, and Technology, MEST) (no. 2007-0054934)