Fecha de publicación: 20/11/2024 Fuente: Microorganisms - Revista científica (MDPI) Microorganisms, Vol. 12, Pages 2366: Recombinant SAG2A Protein from Toxoplasma gondii Modulates Immune Profile and Induces Metabolic Changes Associated with Reduced Tachyzoite Infection in Peritoneal Exudate Cells from Susceptible C57BL/6 Mice
Microorganisms doi: 10.3390/microorganisms12112366
Authors:
Thaíse Anne Rocha dos Santos
Mário Cézar de Oliveira
Edson Mario de Andrade Silva
Uener Ribeiro dos Santos
Monaliza Macêdo Ferreira
Ana Luísa Corrêa Soares
Neide Maria Silva
Tiago Antônio de Oliveira Mendes
Jamilly Azevedo Leal-Sena
Jair Pereira da Cunha-Júnior
Tiago Wilson Patriarca Mineo
José Roberto Mineo
Érica Araújo Mendes
Jane Lima-Santos
Carlos Priminho Pirovani

Toxoplasmosis is a neglected disease that represents a significant public health problem. The antigenic profile of T. gondii is complex, and the immune response can lead to either susceptibility or resistance. Some antigens, such as surface antigen glycoprotein (SAG), are expressed on the surface of tachyzoite stages and interact with the host immune cells. In this study, we investigated the potential of the recombinant SAG2A protein of T. gondii to control parasitism and modulate the immune response in the peritoneal exudate cells (PECs) of both susceptible (C57BL/6) and resistant (BALB/c) mice using an in vitro infection model, gene expression, proteomic analysis, and bioinformatic tools. Our results showed that rSAG2A-treated PECs presented a lower parasitism in C57BL/6 mice but not in the PECs from BALB/c mice, and induced a pro-inflammatory cytokine profile in C57BL/6 mice (iNOS, TNF-α, and IL-6). rSAG2A modulated different exclusive proteins in each mouse lineage, with PECs from the C57BL/6 mice being more sensitive to modulation by rSAG2A. Additionally, biological processes crucial to parasite survival and immune response were modulated by rSAG2A in the C57BL/6 PECs, including fatty acid beta-oxidation, reactive oxygen species metabolism, interferon production, and cytokine-mediated signaling pathways. Together, our study indicates that rSAG2A controls T. gondii parasitism in susceptible C57BL/6 PECs through the modulation of pro-inflammatory cytokines and enhanced expression of proteins involved in the cytotoxic response.