Treatment for toxoplasmosis is not completely successful because of their unwanted side effects, and new treatments are needed. Imiquimod has ability to moderate immune response and used to treat a wide variety of infections and tumors. The aim of the present study was to evaluate the effect of imiquimod on the tachyzoites of T. gondii and infected macrophages in vitro and in BALB/c mice. The viability of T. gondii was assessed in the presence of various concentrations of imiquimod by direct counting after 6 and 24 h. The MTT assay was used to identify the viability of uninfected macrophages. The apoptotic effects were determined with flow cytometry on the tachyzoites and infected macrophages. For evaluation of parasite load in pre-treatment or post-treatment of macrophages Quantitative real time PCR (qPCR) was performed. For in vivo experiments, BALB/c mice received imiquimod before and after challenge with parasites. The mortality rate of mice, parasite numbers in spleen, and the INF-γ and IL-4 cytokine levels in spleen lymphocytes were evaluated. Imiquimod demonstrated anti-Toxoplasma effects by reducing the number of tachyzoites. The results of flow cytometry for drug-treated tachyzoites showed that apoptosis did not rise significantly relative to the control group (p < 0.05). Moreover, apoptosis was enhanced in infected macrophages as the concentration of imiquimod was reduced. The parasitic burden in imiquimod pretreated macrophages was significantly lower than those treated after infection (p < 0.01). A marked reduction was observed in survival rate, parasite load and INF-γ level in BALB/c mice that received imiquimod before parasitic challenge relative to those received drug after parasitic challenge (p < 0.01). Overall, imiquimod in the pretreated group had greater anti-Toxoplasma effects than imiquimod in posttreated group in vitro and in vivo. imiquimod may be considered as a candidate for use against Toxoplasmosis both therapeutically and prophylactically.

弓形虫病的治疗由于其不良的副作用而不能完全成功，因此需要新的治疗方法。咪喹莫特具有调节免疫反应的能力，可用于治疗多种感染和肿瘤。本研究的目的是评估咪喹莫特对速殖子的速殖子的影响。弓形虫 和感染的巨噬细胞 体外和BALB / c小鼠中。的生存能力弓形虫通过在6和24小时后直接计数，在存在各种浓度的咪喹莫特的情况下评估药物浓度。MTT测定法用于鉴定未感染的巨噬细胞的生存力。用流式细胞仪测定速殖子和被感染的巨噬细胞的凋亡作用。为了评估巨噬细胞的预处理或后处理中的寄生虫负荷，进行了定量实时PCR（qPCR）。对于体内实验中，BALB / c小鼠在用寄生虫攻击之前和之后都接受了咪喹莫特。评价小鼠的死亡率，脾脏中的寄生虫数量以及脾脏淋巴细胞中的INF-γ和IL-4细胞因子水平。咪喹莫特证明了抗弓形虫通过减少速殖子的数量来达到效果。药物处理的速殖子的流式细胞术结果表明，相对于对照组，细胞凋亡没有明显增加（p<0.05）。此外，随着咪喹莫特浓度的降低，凋亡在感染的巨噬细胞中增强。咪喹莫特预处理的巨噬细胞的寄生虫负担明显低于感染后处理的巨噬细胞（p<0.01）。与寄生虫攻击后接受药物的BALB / c小鼠相比，寄生虫攻击前接受咪喹莫特的存活率，寄生虫负荷和INF-γ水平明显降低（p<0.01）。总体而言，预处理组咪喹莫特具有更大的抗弓形虫 后治疗组比咪喹莫特治疗效果好 体外 和 体内。咪喹莫特可以被认为是治疗和预防弓形虫病的候选药物。