Different parasite inocula determine the modulation of the immune response and outcome of experimentalTrypanosoma cruziinfection

摘要: Summary During infection, the host response develops effector mechanisms to combat parasite. However, this can become uncontrolled or regulated by that modulate inflammatory reaction. The number of parasites infects host, such as trypomastigotes in Chagas disease, may also influence immune activation and disease pathology. We evaluated inflammation regulation follows Trypanosoma cruzi infection with low (300), intermediate (3000) high (30 000) parasite loads. Our results showed load inoculum influenced outcome: higher inoculum, lower were survival rates. There was a strong association between parasitism infiltrate heart determined cytokine interplay tissue, shown increased interferon-γ, tumour necrosis factor-α, interleukin-17 (IL-17) IL-23 300 30 000 groups, IL-4 IL-10 intermediate-inoculum mice, elevated IL-6 production mice 3000 groups. T cells antigen-presenting augmented infected especially for splenic CD4+ CD25+ regulatory expressing CD45RBlow, GITR, PD-1 FoxP3 group highest inoculum. Interestingly, these presented an apparent decrease CD4+ CD25+ FoxP3+ cardiac infiltrate, contrast group, which numbers leucocytes heart. Finally, our demonstrated during T. cruzi is linked pattern will result parasite/inflammation control tissue damage.