Details

Autor(en) / Beteiligte

• 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

Titel

The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response

Ist Teil von

• Frontiers in immunology, 2020-06, Vol.11, p.1010-1010

Ort / Verlag

Switzerland: Frontiers Research Foundation

Erscheinungsjahr

2020

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• 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 parasitism during acute experimental infection is unclear. We observed that recombinant P21 (rP21) decreased the multiplication of 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, produced more P21. The effect of P21 in controlling the replication of , 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 latency in the host organism, enabling the protozoan to evade the host's immune system.