ABSTRACT
In humans infected with Echinococcus multilocularis, larval metacestodes will develop, proliferate and progressively infiltrate the surrounding host tissues by exogenous budding of parasitic microvesicles or cell lines which detach from the original tumour and thus become transported through blood or lymph vessels into other organs. Cellular effector mechanisms constitute the most effective means to restrict parasite persistence and proliferation, and here we demonstrate that E. multilocularis vesicle antigens will induce pro-inflammatory, regulatory and chemokine release by PBMC from patients. The pro-inflammatory cytokines IL-1beta and IL-18 were reduced in echinococcosis patients, regulatory IL-10 was similar, but parasite vesicle-induced IL-8 was dominant and clearly elevated in patients. Such selective and opposite dynamics of inflammatory cytokines and chemokine release may prevent overwhelming and pathogenic inflammation, and constitute an appropriate response for attraction of effector cells into the periparasitic tissues with the capacity to limit E. multilocularis metacestode proliferation and dissemination.
