Biotherapy of mice’s serum 13cH modifies parasitological and immunological parameters of Trypanosoma cruzi infection.

Background: T. cruzi biotherapies’ alter the infection course by this protozoan [1,2], fact that encourages the evaluation of other highly diluted medicines which modulates host’s immune system. Aim: Evaluate effect of biotherapy produced from mices’s serum in experimental infection by T. cruzi. Methodology: A blind, randomized and controlled study was performed. Animals: 60 male Swiss mice, four weeks old were inoculated intraperitoneally with 1400 trypomastigotes-Y strain and divided: MNI: mice non-infected by T. cruzi; IC: treated with hydroalcoholic solution 7%; BSI13cH: treated with mice’s serum infected by T. cruzi 13cH. Biotherapies: produced from mice’s serum infected by T. cruzi in 13cH dynamization [3]. Treatment: mice were treated 48 hours before and after infection. Subsequently animals were treated 56/56 hours until 9th day of infection (d.i). The medicine was diluted in water (1/100mL) and offered ad libitum, for 16 hours. Parasitological parameters: were evaluated pre-patent and patent period, parasitemia peak, total parasitemia and mortality [4]. Cytokine dosage: IL-4, IL-17, TNF-α and IFN-γ were measured in serum on 0, 8th and 12th d.i., by enzyme immunoassay. Ethics: study was approved by Ethics Committee for Experiments in Animals/UEM. Statistic: data were compared with Mann Whitney or Student t test, significance 5%. Results: BSI13cH showed tendency to increase total parasitemia (p=0.06) and parasitemia peak (p=0.05), with lower patent period (p=0.03) and higher mortality (p=0.03) compared to IC. In dosage of cytokines BSI13cH group showed on 0 d.i. a decrease in IL-17 (p = 0.02) and increased IL-4 (p = 0.01) compared to MNI (baseline value), probably caused by modulation of medication administration 48 hours before infection. IL-17 concentration didn’t vary throughout the infection to BSI13cH, different IC that tended to decrease concentration of cytokine on 8th d.i. IL-4 increased significantly on 0 d.i. to BSI13cH, with subsequent return to baseline values. IC group didn’t change significantly IL-4 value along the infection. IFN-γ concentration on 12th d.i. to BSI13cH was lower (p = 0.00) than IC, which increased this cytokine on 8th and 12th di. TNF-α concentration of BSI13cH followed the same evolution as IC, with an increase on 8th and 12th d.i. (Figure 1). The medicine seems initially promote Th2 response (IL-4), hindering the development of effective Th1 response (INF-γ), causing an increase of parasitemia and animals' death. Conclusions: BSI13cH demonstrated effect in experimental infection by T. cruzi with increased parasitemia, animals’ premature death and modulated immune response differently of IC.