Immuno-modulatory activity of Ganoderma lucidum-derived polysacharide on human monocytoid dendritic cells pulsed with Der p 1 allergen

PS-G induced the maturation of MD-DCs and decreased phagocytic capacity, even if pulsed with Der p 1. After incubation with PS-G and Der p 1, MD-DCs produced higher amounts of IL-12 p70, IL-12 p40, IL-6, IL-23, and IL10 than Der p 1-pulsed DCs. Furthermore, type 1 helper T (Th1) cell cytokine (INF-γ) production was highly increased when na？ve autologous T cells were co-cultured with Der p 1-pulsed MD-DCs. Na？ve T cells stimulated by MD-DCs pulsed with Der p 1 failed to produce proliferation of T-cells, whereas the addition of PS-G to Der p 1 induced a significant proliferation of T-cells similar to that observed with PS-G alone.The presence of PS-G in an allergen pulse promoted allergic MD-DCs to produce IL-12 p70, IL-12 p40, IL-6, IL-23, and IL-10, and exerted an effect on shifting the immune balance towards Th1 in children with allergic asthma.Allergic asthma is a common childhood disease that often persists into adulthood. The prevalence of childhood allergic diseases has increased dramatically in recent decades in many parts of the world [1], and children who mount an immune response to inhalant allergens have an increased risk of developing asthma. This immune response includes both IgE antibodies and type 2 helper T (Th2) cells, which are thought to contribute to inflammation in the respiratory tract. Moreover, sensitization to indoor allergens (dust mites, cats, and dogs) is strongly associated with asthma. The allergic disorders and diseases are characterized by predominant Th2 cytokine (IL-4, IL-5, and IL-13) production [2].Ganoderma lucidum, a medicinal mushroom, is among the most popular herbal medicines in East Asia. G. lucidum has been reported to be effective in modulating immune functions, inhibiting tumor growth, and in the treatment of chronic hepatopathy, hypertension, neoplasia, and hyperglycemia [3-5]. G. lucidum has also been used to prevent and treat atopic diseases in several mouse and human models [6-8]. The main functional components of G. l