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. 2017 Aug 2;8:840. doi: 10.3389/fimmu.2017.00840

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Copyright © 2017 Nascimento, Andrade, Carvalho-Pinto, Serra, Vellasco, Brasil, Ramos-Junior, da Mota, Almeida, Andrade, Correia Soeiro, Juliano, Alvarenga, Oliveira, Sicuro, de Carvalho, Svensjö and Scharfstein.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Activation of the kallikrein–kinin system fuels heart parasitism. Measurements of Trypanosoma cruzi DNA (3 d.p.i.) in the heart of C57BL/6 infected [10⁶ tissue culture trypomastigotes (TCTs)] intracardiacally (A,C,D), WT (B6-Kit^+/+) mice or mast cell deficient (B6-kitW-sh/W-sh) mice (B). Where indicated, the mice were pretreated with cromoglycate, B2R antagonist (B2RA) (HOE-140), endothelin A receptor (ET_AR)/endothelin B receptor (ET_BR) double antagonist (bosentan) or factor XII (FXII) inhibitor (infestin-4). Results (mean ± SD) of T. cruzi DNA by quantitative polymerase chain reaction (qPCR) are representative of two independent experiments (five mice/group). Statistical analyzes were done by analysis of variance with Bonferroni post test (*P < 0.05; **P < 0.01, ***P < 0.001).