Ganoderma tsugae in vivo modulates Th1/Th2 and macrophage responses in an allergic murine model

We have reported that Ganoderma tsugae supplementation alleviates bronchoalveolar inflammation in an airway sensitization and challenge model with female BALB/c mice. However, the effects of G. tsugae supplementation in vivo on serum antibody levels, splenocyte and peritoneal microphage immune responses have not yet been determined. In this study, serum antibody levels, cytokines and splenocyte chemical mediators and peritoneal macrophage cultures from ovalbumin (OVA)-sensitized and -challenged mice were examined after continuously consuming G. tsugae supplementation diets for 5 weeks. The results showed that OVA sensitization and challenge significantly (P < 0.05) decreased the spontaneous production of IL-2 (Th1) cytokine, but significantly (P < 0.05) increased spontaneous and OVA-stimulated IL-4 (Th2) production in splenocyte cultures from experimental mice. OVA administration significantly decreased both spontaneous and LPS/IFN-gamma-stimulated IL-1 beta and IL-6 levels in peritoneal macrophage cultures from experimental mice. However, dietary supplementation with G. tsugae significantly increased spontaneous IL-2 level, but slightly decreased spontaneous IL-4 level in cultured splenocyte supernatants in the experimental groups. G. tsugae supplementation enhanced pro-inflammatory cytokines IL-1 beta and IL-6 production in cultured peritoneal macrophages. However, the nitric oxide level from cultured peritoneal macrophages and serum OVA-specific IgE and IgG(2a) antibody levels was not significantly affected. These results suggest that OVA sensitization and challenge induced a Th2-skewed splenocyte response and decreased peritoneal macrophage cytokine secretion. G. tsugae supplementation in vivo modulated the Th1/Th2 balance and enhanced macrophage immune responses. However, the supplementation diet could not fully reverse the Th2-skewed responses to level of Th1-skewed responses. (c) 2006 Elsevier Ltd. All rights reserved.