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Different parasite inocula determine the modulation of the immune response and outcome of experimental T rypanosoma cruzi infection
Author(s) -
Borges Diego C.,
Araújo Natalia M.,
Cardoso Cristina R.,
Lazo Chica Javier E.
Publication year - 2013
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12022
Subject(s) - immune system , biology , trypanosoma cruzi , parasite hosting , foxp3 , parasite load , inflammation , immunology , chagas disease , microbiology and biotechnology , il 2 receptor , cytokine , tumor necrosis factor alpha , interleukin 10 , effector , antigen , interleukin , pathogen , t cell , world wide web , computer science
Summary During infection, the host response develops effector mechanisms to combat the parasite. However, this response can become uncontrolled or regulated by mechanisms that modulate the inflammatory reaction. The number of parasites that infects the host, such as trypomastigotes in Chagas disease, may also influence immune activation and disease pathology. We evaluated the inflammation and immune regulation that follows Trypanosoma cruzi infection with low (300), intermediate (3000) or high (30 000) parasite loads. Our results showed that the load of parasite inoculum influenced disease outcome: the higher the number of parasites in the inoculum, the lower were the survival rates. There was a strong association between parasitism and inflammatory infiltrate in the heart and the parasite inoculum determined cytokine interplay in this tissue, as shown by increased interferon‐γ, tumour necrosis factor‐α, interleukin‐17 ( IL ‐17) and IL ‐23 in the 300 and 30 000 inoculum groups, higher IL ‐4 and IL ‐10 in the intermediate‐inoculum mice, and elevated IL ‐6 production in the heart of mice in the 3000 and 30 000 groups. The number of T cells and antigen‐presenting cells was augmented in the infected groups, especially for the splenic CD 4 + CD 25 + regulatory T cells expressing CD 45 RB low , GITR , PD ‐1 and FoxP 3 in the group with the highest inoculum. Interestingly, these mice also presented an apparent decrease in CD 4 + CD 25 + FoxP 3 + cells in the cardiac infiltrate, in contrast to the intermediate inoculum group, which showed elevated numbers of these regulatory leucocytes in the heart. Finally, our results demonstrated that parasite load during T . cruzi infection is linked to the response pattern that will result in parasite/inflammation control or tissue damage.