Abstract
Abstract CD4+CD25+Foxp3+ regulatory T cell (Treg) plays an important role in immune tolerance which can reduce inflammation and allergic reactions through its inhibitory functions. Bee venom (BV) has been widely used in the treatment of chronic inflammatory diseases such as Rheumatoid Arthritis. In this study, we hypothesized that phospholipase A2 (PLA2), major constituent of BV, could increase Treg expression and treat OVA-induced allergic asthma in mice. In vitro study, the percentage of Treg increased significantly by PLA2 treatment in CD4+T cell compared to saline treatment. In OVA induced allergic asthma model, PLA2-treatment significantly suppressed eosinophil and lymphocyte infiltration in BALF. In addition, PLA2 inhibited the production of IL-4, IL-13, INF-γ, IgE and OVA-specific IgE, along with suppressing airway hyper-responsiveness. Furthermore, CD4+CD25+Foxp3+ population was significantly increased by PLA2 treatment. Interestingly, these anti-asthmatic effects by PLA2 were totally abolished by Treg depletion via anti-CD25 antibody injection, suggesting pharmaceutical action of PLA2 was medicated by Treg. Our data suggest that PLA2 inhibits OVA-induced allergic airway inflammation by modulating Treg function.
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