Toxoplasma gondii is a parasite able to infect various cell types, including trophoblast cells. Studies have demonstrated that interleukin (IL)-10, transforming growth factor (TGF)-β1 and interferon (IFN)-γ are involved in the susceptibility of BeWo trophoblast cells to T. gondii infection. Furthermore, T. gondii is able to adhere to the plasma membrane of host cells through intercellular adhesion molecule (ICAM)-1. Thus, the present study aimed to assess the role of IL-10, TGF-β1 and IFN-γ in the expression of ICAM-1 in BeWo and HeLa cells and to analyze the role of ICAM-1 in the adhesion and invasion of T. gondii to these cells under the influence of these cytokines. For this purpose, BeWo and HeLa cells were treated or not, before and after T. gondii infection, with rIL-10, rTGF-β1 or rIFN-γ. For the BeWo cells, rIL-10 and rTGF-β1 favored susceptibility to infection, but only rTGF-β1 and rIFN-γ increased ICAM-1 expression, and TNF-α release. On the other hand, rIFN-γ downregulated the expression of ICAM-1 triggered by T. gondii in HeLa cells, leading to control of the infection. Moreover, we observed that upregulation of ICAM-1, mediated by cytokine's stimulation, in BeWo and HeLa cells resulted in a high number rate of both parasite adhesion and invasion to these cells, which were strongly reduced after ICAM-1 neutralization. Likewise, the blockage of ICAM-1 molecule also impaired T. gondii infection in human villous explants. Taken together, these findings demonstrate that TGF-β1 and IFN-γ differentially regulate ICAM-1 expression, which may interfere in the adhesion/invasion of T. gondii to BeWo and HeLa cells for modulating susceptibility to infection.

弓形虫是一种能够感染各种细胞类型的寄生虫，包括滋养层细胞。研究表明，白细胞介素 (IL)-10、转化生长因子 (TGF)-β1 和干扰素 (IFN)-γ 与 BeWo 滋养层细胞对弓形虫感染的易感性有关。此外，弓形虫能够通过细胞间粘附分子 (ICAM)-1 粘附到宿主细胞的质膜上。因此，本研究的目的是评估IL-10的作用，TGF-β1和IFN-γ在ICAM-1的中的BeWo和HeLa细胞中的表达来分析的粘附和入侵ICAM-1的作用Ť . gondii在这些细胞因子的影响下对这些细胞产生影响。为此，BeWo 和 HeLa 细胞在之前和之后进行了处理或未处理弓形虫感染，带有 rIL-10、rTGF-β1 或 rIFN-γ。对于 BeWo 细胞，rIL-10 和 rTGF-β1 有利于感染易感性，但只有 rTGF-β1 和 rIFN-γ 增加 ICAM-1 表达和 TNF-α 释放。另一方面，rIFN-γ 下调HeLa 细胞中由弓形虫触发的 ICAM-1 的表达，从而控制感染。此外，我们观察到 BeWo 和 HeLa 细胞中由细胞因子刺激介导的 ICAM-1 上调导致寄生虫对这些细胞的粘附和侵袭的高数量率，在 ICAM-1 中和后显着降低。同样，ICAM-1 分子的阻断也损害了弓形虫在人绒毛外植体中感染。综上所述，这些发现表明 TGF-β1 和 IFN-γ 差异调节 ICAM-1 的表达，这可能会干扰弓形虫对 BeWo 和 HeLa 细胞的粘附/侵袭，以调节对感染的易感性。