Image_1_The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response.jpg (1.35 MB)
Download file

Image_1_The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response.jpg

Download (1.35 MB)
figure
posted on 05.06.2020, 11:48 authored by Flávia Alves Martins, Marlus Alves dos Santos, Júlia de Gouveia Santos, Aline Alves da Silva, Bruna Cristina Borges, Mylla Spirandelli da Costa, Paula Cristina Brígido Tavares, Samuel Cota Teixeira, Rebecca Tavares e Silva Brígido, Thaise Lara Teixeira, Cassiano Costa Rodrigues, Nadjania Saraiva de Lira Silva, Rayane Cristina de Oliveira, Laura Caroline de Faria, Marcela Rezende Lemes, Renata Graciele Zanon, Tatiana Carla Tomiosso, Juliana Reis Machado, Marcos Vinicius da Silva, Carlo José Freire Oliveira, Claudio Vieira da Silva

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.

History

References