Aqueous extracts from Menyanthes trifoliate and Achillea millefolium affect maturation of human dendritic cells and their activation of allogeneic CD4+ T cells in vitro.
Palabras clave
Abstracto
BACKGROUND
Menyanthes trifoliate and Achillea millefolium have been used in traditional medicine to ameliorate chronic inflammatory conditions. The aim of this study was to identify the effects of ethanol and aqueous extracts of Menyanthes trifoliate and Achillea millefolium on maturation of dendritic cells (DCs) and their ability to activate allogeneic CD4(+) T cells.
METHODS
Human monocyte-derived DCs were matured in the absence or presence of lyophilised aqoueous or ethanol extracts from Menyanthes trifoliate or Achillea millefolium and their expression of surface molecules analysed with flow cytometry and cytokine secretion measured by ELISA. DCs matured in the presence of aqueous extracts from Menyanthes trifoliate and Achillea millefolium were co-cultured with allogeneic CD4(+) T cells and the expression of surface molecules by T cells and their cytokine secretion and cell proliferation determined.
RESULTS
Maturation of DCs in the presence of aqueous extracts from Menyanthes trifoliate or Achillea millefolium did not affect expression of the surface molecules examined but reduced the ratio of secreted IL-12p40/IL-10, compared with that by DCs matured in the absence of extracts. Allogeneic CD4(+) T cells co-cultured with DCs matured in the presence of aqueous extract from Menyanthes trifoliate secreted less IFN-γ, IL-10 and IL-17 than CD4(+) T cells co-cultured with DCs matured without an extract. Maturation of DCs in the presence of aqueous extract from Achillea millefolium decreased IL-17 secretion but did not affect IFN-γ and IL-10 secretion by allogeneic CD4(+) T cells.
CONCLUSIONS
Aqueous extract from Menyanthes trifoliate induces a suppressive phenotype of DCs that has reduced capacity to induce Th1 and Th17 stimulation of allogeneic CD4(+) T cells, whereas aqueous extract from Achillea millefolium reduces the capacity of DCs to induce a Th17 response.
