Fig. 13

Schematic model representing T. gondii infection in C57BL/6 mice and the influence of SGE treatment on cytokine release in serum and the small intestine. Our data demonstrate that T. gondii infection increases the levels of inflammatory cytokines such as TNF and IFN-γ in both mouse serum and small intestine tissue. Additionally, animals treated with the highest concentration of SGE experienced less weight loss and lower clinical scores. Specifically, mice treated with SGE 30 µg exhibited a significant increase in systemic regulatory cytokines, including IL-4, IL-2, and IL-10, during the chronic phase of infection. Cytokine analysis further revealed that SGE-treated mice secreted more intestinal IL-4 in the chronic phase and increased levels of IL-2 and IL-22 in the acute phase. Moreover, cyst counts indicated that SGE-treated groups had significantly fewer cysts in brain tissue compared to the untreated group. Therefore, our findings demonstrate that SGE has the ability to induce a regulatory response, mitigating the detrimental effects of uncontrolled inflammation and providing protection against T. gondii infection