AUTHOR=Martins Flávia Alves , dos Santos Marlus Alves , Santos Júlia de Gouveia , da Silva Aline Alves , Borges Bruna Cristina , da Costa Mylla Spirandelli , Tavares Paula Cristina Brígido , Teixeira Samuel Cota , Brígido Rebecca Tavares e Silva , Teixeira Thaise Lara , Rodrigues Cassiano Costa , Silva Nadjania Saraiva de Lira , de Oliveira Rayane Cristina , de Faria Laura Caroline , Lemes Marcela Rezende , Zanon Renata Graciele , Tomiosso Tatiana Carla , Machado Juliana Reis , da Silva Marcos Vinicius , Oliveira Carlo José Freire , da Silva Claudio Vieira TITLE=The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response JOURNAL=Frontiers in Immunology VOLUME=11 YEAR=2020 URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2020.01010 DOI=10.3389/fimmu.2020.01010 ISSN=1664-3224 ABSTRACT=

Trypanosoma cruzi P21 protein (P21) is a putative secreted and immunomodulatory molecule with potent bioactive properties such as induction of phagocytosis and actin cytoskeleton polymerization. Despite the bioactive properties described so far, the action of P21 on parasite replication in muscle cell lineage or T. cruzi parasitism during acute experimental infection is unclear. We observed that recombinant P21 (rP21) decreased the multiplication of T. cruzi in C2C12 myoblasts, phenomenon associated with greater actin polymerization and IFN-γ and IL-4 higher expression. During experimental infection, lower cardiac nests, inflammatory infiltrate and fibrosis were observed in mice infected and treated with rP21. These results were correlated with large expression of IFN-γ counterbalanced by high levels of IL-10, which was consistent with the lower cardiac tissue injury found in these mice. We have also observed that upon stress, such as that induced by the presence of the IFN-γ cytokine, T. cruzi produced more P21. The effect of P21 in controlling the replication of T. cruzi, may indicate an evolutionary mechanism of survival developed by the parasite. Thus, when subjected to different stress conditions, the protozoan produces more P21, which induces T. cruzi latency in the host organism, enabling the protozoan to evade the host's immune system.