摘要：

Top of page1 Introduction 2 Results 3 Discussion 4 Materials and methods Acknowledgements To elucidate the roles of neutrophils in experimental Chagas' disease, we depleted the peripheral neutrophils in BALB/c and C57BL/6 mice with a monoclonal antibody 1 day before Trypanosoma cruzi infection. Neutrophil depletion in BALB/c mice resulted in exacerbation of the disease and decreased expression of mRNA for Th1 cytokines, including IL-2 and IFN-γ, IL-12p40 and TNF-α in their spleens after the infection, while a Th2 cytokine, IL-10, increased especially 1 day after infection. Neutrophils from infected BALB/c mice expressed mRNA for IL-12p40, IFN-γ, TNF-α and Th1 chemoattractive chemokines, monokine induced by IFN-γ (MIG) and macrophage inflammatory protein-1α (MIP-1α). In contrast, in C57BL/6 mice neutrophil depletion induced resistance to the disease and enhanced the expression of the above Th1 cytokines, although IL-10 mRNA in neutrophil-depleted C57BL/6 mice was also higher than in control mice. Neutrophils from C57BL/6 mice did not express IL-12p40, IFN-γ and MIG but expressed TNF-α, MIP-1α and IL-10. Therefore, neutrophils may play opposite roles in these two strains of mice with respect to protection versus exacerbation of T.cruzi infection, possibly through modulating the Th1/Th2 dichotomy in different directions.

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